GATA1 is a zinc-finger transcription factor that recognizes GATA-containing regulatory DNA and organizes context-dependent transcriptional complexes in the nucleus. It activates and represses RNA polymerase II target genes during erythroid and megakaryocytic differentiation and helps specify eosinophil fate. Interactions with FOG1 and other cofactors couple DNA recognition to lineage-specific gene expression. Alternative translation initiation produces GATA1s, which lacks the N-terminal transactivation region. Short-form-only states impair human erythropoiesis and occur in Down-syndrome-associated transient abnormal myelopoiesis and acute megakaryoblastic leukemia.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000981 DNA-binding transcription factor activity, RNA polymerase II-specific | IBA GO_REF:0000033 | ACCEPT | Summary: GATA1 is a DNA-binding transcription factor with activating and repressive PolII outputs. Reason: Direct promoter binding is coupled to transcriptional activation of erythroid genes and repression at selected loci. Actual PAINT target descent and exact canonical sequence support the inherited transcription-factor activity. The unpolarized term remains appropriate because both activation and repression are established; the source is not weakened by its legitimate target-containing donor list. |
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: GATA1 functions in the nucleus, as inherited across the verified GATA family clade. Reason: The actual PAINT tree places the exact 413-residue human target beneath the nucleus IBD origin, with the target’s own evidence legitimately among the descendant sources. Direct GATA1 nuclear localization and chromatin experiments independently agree. Retain the broad nucleus term under the root-organelle convention alongside nucleoplasm; this is not an exclusive localization claim or a rejection of the considered ancestral placement. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: Conserved GATA-family sequence recognition supports GATA1 binding to PolII cis-regulatory DNA. Reason: The two zinc-finger transcription factor recognizes erythroid regulatory motifs, corroborated by human promoter binding and chromatin occupancy studies. Actual PAINT evidence places the assertion at an ancestral node whose descendants include the exact canonical human GATA1 sequence; no target-specific loss was found. The target appearing among experimental descendants is legitimate phylogenetic support, not circularity. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: The actual GATA-family phylogeny supports positive PolII transcriptional regulation. Reason: The human target inherits this IBD on the verified ancestral path, and its own experimental evidence is legitimate descendant support. Direct human promoter activation independently agrees. The dated upstream donor-list difference is retained in provenance and is not presented as a loss of the family placement or circular evidence. |
| GO:0000122 negative regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: GATA1 can repress PolII transcription through promoter binding and coregulators. Reason: The actual PAINT IBD lies on the verified ancestral path to the human target, and the target’s own descendant evidence is legitimate support. Original human K562 ZNF268 experiments directly demonstrate GATA1-dependent promoter repression, complementing its activating functions. Retain the ancestral repressive role without treating donor count or self-inclusion as weakness. |
| GO:0045165 cell fate commitment | IBA GO_REF:0000033 | ACCEPT | Summary: GATA1 helps establish hematopoietic lineage identity. Reason: GATA1 helps establish erythroid, megakaryocytic and eosinophil lineage identity. The conserved cell-fate assertion is placed at AN3/PTN000800998, on the verified human target lineage, and is supported by original lineage experiments including eosinophil commitment. Retain this cross-lineage core role: the specific eosinophil commitment annotation covers one lineage rather than replacing the full biological scope. In contrast, the broad anatomical-morphogenesis annotation is retained only through the already represented platelet-formation program and adds no distinct scope. |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000120 | MODIFY | Summary: GATA1 is a DNA-binding transcription factor acting at PolII-regulated genes. Reason: The family/rule assignment is consistent with direct promoter recognition, transcriptional activation and repression in human erythroid systems. The verified PolII-specific descendant GO:0000981 adds the established polymerase context to the generic transcription-factor term. Both activating and repressive outputs remain represented; the refinement does not assign a chromatin-enzyme activity to GATA1. Proposed replacements: DNA-binding transcription factor activity, RNA polymerase II-specific |
| GO:0005634 nucleus | IEA GO_REF:0000120 | ACCEPT | Summary: The electronic nucleus annotation agrees with direct nuclear evidence. Reason: The literal ortholog and subcellular-location mappings are retained. Independent original nuclear localization and promoter-occupancy experiments support the nucleus as the central site of GATA1 transcriptional action. The accepted root-organelle term remains valid alongside the more specific nucleoplasm annotation, without converting donor fields into human experimental records. |
| GO:0005654 nucleoplasm | IEA GO_REF:0000117 | ACCEPT | Summary: The ARBA nucleoplasm assignment agrees with direct GATA1 biology. Reason: GATA1 binds nuclear cis-regulatory DNA and recruits transcriptional coregulators. Human K562 chromatin and transcription experiments support the rule-based nucleoplasmic location. Preserve the literal ARBA identifier, and do not interpret this location as evidence that every mapped complex has been independently purified in human cells. |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000002 | MODIFY | Summary: GATA1 regulates transcription of PolII genes. Reason: The conserved GATA DNA-binding domains are consistent with direct activation and repression at human globin and ZNF268 promoters. Refine the generic DNA-templated-transcription regulation label to verified descendant GO:0006357, which supplies the established polymerase context without imposing one regulatory direction on all targets. Proposed replacements: regulation of transcription by RNA polymerase II |
| GO:0006357 regulation of transcription by RNA polymerase II | IEA GO_REF:0000120 | ACCEPT | Summary: GATA1 directly regulates PolII transcription in erythroid programs. Reason: The ARBA/InterPro assignment agrees with direct human promoter binding, chromatin occupancy and transcriptional activation or repression. GATA1 performs the regulatory work through DNA recognition and partner recruitment; this is not merely expression correlated with a downstream phenotype. Both signs of regulation remain represented in the specific annotations. |
| GO:0008270 zinc ion binding | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: Zinc coordination stabilizes the GATA DNA-binding fingers. Reason: The InterPro mapping reflects the conserved zinc-finger architecture recorded in the genuine GATA1 sequence and reviewed protein record. Structural zinc binding is chemically appropriate, but it is a supporting feature of the transcription-factor fold rather than the most informative standalone core molecular function. Retain it as non-core without implying a catalytic metal-dependent activity or rejecting the family assignment. Supporting Evidence: GO_REF:0000002 UniProt:P15976 |
| GO:0009653 anatomical structure morphogenesis | IEA GO_REF:0000117 | TOO GENERAL | Summary: The broad morphogenesis term is true but subsumed by the retained platelet-formation program. Reason: GATA1 supports the megakaryocytic platelet-formation program, including the morphological production of platelets. The verified ontology path is platelet formation (GO:0030220) part_of platelet morphogenesis (GO:0036344), which is_a cell morphogenesis (GO:0000902), itself is_a anatomical structure morphogenesis (GO:0009653). The original ARBA assertion is true, but this ancestor adds no biological specificity beyond the retained platelet-formation annotation. TOO_GENERAL records that redundancy rather than a false electronic assertion. |
| GO:0030154 cell differentiation | IEA GO_REF:0000117 | MODIFY | Summary: GATA1 directs several defined hematopoietic differentiation programs. Reason: The generic ARBA cell-differentiation label is biologically correct but can be expressed as the verified erythrocyte, megakaryocyte and eosinophil differentiation descendants. Human disease and erythroid assays support the first two programs, and the original human CD34-positive transduction and mouse rescue study supports eosinophil differentiation and fate. These replacements preserve multiple genuine lineages rather than reducing GATA1 to one lineage or inventing an additional annotation. Proposed replacements: erythrocyte differentiation megakaryocyte differentiation eosinophil differentiation |
| GO:0043565 sequence-specific DNA binding | IEA GO_REF:0000120 | MODIFY | Summary: The conserved sequence-specific DNA binding acts at PolII cis-regulatory elements. Reason: Human gamma-globin and ZNF268 promoter experiments establish the regulatory location and sequence specificity. Refine the broad electronic sequence-specific DNA-binding annotation to verified descendant GO:0000978 while retaining its mouse/rat and domain-source fields. Ortholog provenance is not recast as a directly assayed human construct. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0048731 system development | IEA GO_REF:0000117 | MARK AS OVER ANNOTATED | Summary: The broad system-development mapping is less well grounded than the specific blood-cell programs. Reason: GATA1’s established direct work controls hematopoietic cell differentiation and maturation. The reviewed target evidence does not establish a separate developmental program of a whole interacting organ or tissue system merely from these cellular outcomes. Mark this generic ARBA assertion as over-annotated while retaining the specific lineage annotations, without denying systemic consequences of GATA1 deficiency. |
| GO:0160108 animal gross anatomical part developmental process | IEA GO_REF:0000117 | MARK AS OVER ANNOTATED | Summary: The gross-anatomical-part developmental label exceeds the target’s demonstrated cellular lineage scope. Reason: The official term concerns development of a gross anatomical part of an animal. GATA1’s direct erythroid, megakaryocytic and eosinophil transcriptional programs establish cell-lineage functions, while the specific gonadal clinical attribution remains uncertain in its original report. Mark this broad ARBA mapping as over-annotated without denying the established hematopoietic roles or systemic disease outcomes. |
| GO:1990837 sequence-specific double-stranded DNA binding | IEA GO_REF:0000117 | MODIFY | Summary: GATA1 recognizes sequence-specific double-stranded DNA in PolII regulatory regions. Reason: The broad ARBA assertion is consistent with direct human promoter and chromatin experiments. GO:0000978 is a verified descendant with the established PolII cis-regulatory context, so refine the function while preserving the original rule identifier. This does not claim that every genomic motif is occupied or transcriptionally regulated in every cell type. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0005515 protein binding | IPI PMID:11675338 X-linked thrombocytopenia caused by a novel mutation of GATA... | MODIFY | Summary: The G208S study tests GATA1 binding to FOG1 zinc fingers. Reason: The authentic PMID:11675338 abstract explicitly reports partial disruption of the GATA1–FOG interaction, especially contact with FOG zinc finger 9. O35615 is the literal mouse FOG1 partner and remains unchanged. The original full assay images were not inspected here, but the positive source statement and independent FOG1 interaction experiments support transcription coregulator binding. This functional refinement preserves the source-specific access and species limits. Proposed replacements: transcription coregulator binding |
| GO:0005515 protein binding | IPI PMID:17132730 The mediator complex functions as a coactivator for GATA-1 i... | MODIFY | Summary: GATA1 recruits the MED1 transcriptional coactivator. Reason: Selected original PMID:17132730 Results/Methods show two-hybrid and GST-pulldown interaction with MED1 fragments, tagged GATA1–Mediator association in mouse erythroid cells, and loss/rescue of GATA-dependent reporter activation in Med1-deficient fibroblasts. Human MED1 rescue constructs are explicit; the GATA1 construct species is not inferred from HeLa extract or recipient cells. The study maps an N-finger requirement, whereas independent PMID:24245781 reports a different domain context; the shared supported claim is coactivator binding, not a universal domain boundary. Proposed replacements: transcription coactivator binding |
| GO:0005515 protein binding | IPI PMID:19513100 Direct binding of pRb/E2F-2 to GATA-1 regulates maturation a... | MODIFY | Summary: GATA1 binds retinoblastoma protein within a cell-cycle regulatory complex. Reason: Selected original PMID:19513100 experiments map human GATA1–pRb binding through the LXCXE motif and distinguish the GATA1–pRb–E2F2 complex from FOG1-containing complexes. P06400 is the literal human RB1 partner. pRb supplies a transcriptional coregulatory role; GO:0001221 captures that supported interaction rather than generic binding. The engineered binding-site mutant and natural short-form comparisons remain distinct, and no GATA1 enzymatic activity is inferred from pRb recruitment. Proposed replacements: transcription coregulator binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:19513100 Direct binding of pRb/E2F-2 to GATA-1 regulates maturation a... | MODIFY | Summary: The mouse pRb partner supports the same conserved coregulator interaction. Reason: P13405 is officially mouse retinoblastoma protein. The original PMID:19513100 study includes separately identified mouse and human GATA1 experiments, biochemical interaction and erythroid GATA1–pRb–E2F2 complex evidence. Retain this mouse-partner record separately from the human RB1 row while specifying transcription coregulator binding. A mouse partner or host is not silently substituted with a human accession, and the engineered mutants are not natural products. Proposed replacements: transcription coregulator binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:19513100 Direct binding of pRb/E2F-2 to GATA-1 regulates maturation a... | MODIFY | Summary: GATA1 binds FOG1 as a transcriptional coregulator in a complex distinct from its pRb interaction. Reason: The literal Q8IX07 partner is human FOG1/ZFPM1. Selected original PMID:19513100 binding and competition experiments show that FOG1 association is distinct from the GATA1–pRb–E2F2 complex; they do not support one combined supercomplex. Transcription coregulator binding captures the demonstrated functional partner role, preserving the source and avoiding an unsupported direct DNA-binding role for FOG1. Proposed replacements: transcription coregulator binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen records GATA1 interaction with FRS3. Reason: The authentic HI-II-14 supplementary interaction table contains the GATA1–FRS3 gene pair, with the retained O43559 accession-to-ORF crosswalk supporting the partner identity. The library contains a GATA1 ORF matching current P15976-2, but the pair table does not assign a clone to each interaction. Retain this positive experimental provenance while removing the uninformative generic protein-binding annotation; it does not establish a GATA1 adaptor activity or a physiological FRS3-dependent process. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen records GATA1 interaction with PRKAB2. Reason: The selected original interaction table and accession crosswalk support the O43741/PRKAB2 pair. Human ORF fusion proteins were tested in yeast; no pair-specific orthogonal or physiological assay is established in the inspected supplement. Remove the generic binding annotation under specificity policy without treating the recorded interaction as false or assigning AMPK regulatory activity to GATA1. The available library GATA1 clone is not promoted to a per-pair isoform assertion. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | MODIFY | Summary: GATA1 binds the sequence-specific transcription factor HOXA1 in the binary screen. Reason: GATA1 binds HOXA1, a sequence-specific PolII DNA-binding transcription factor, supporting GO:0061629 rather than uninformative generic binding. Original HI-II-14 Table S2G records the pair in two discovery screens. Published positive pairs underwent individual quadruplicate retesting, required at least 3/4 positive results, lacked autoactivation on counterselection, and had sequence-confirmed identities. The P49639/ORF crosswalk establishes the partner. No pair-specific orthogonal confirmation or natural-product assignment is retained; this molecular binding claim does not assert a shared physiological developmental program. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen records GATA1 interaction with KRTAP10-5. Reason: The authentic selected table and P60370 accession crosswalk support this positive interaction. A high-throughput binary contact with a keratin-associated protein does not identify an informative GATA1 molecular role. Remove bare protein binding while preserving the actual assay and partner, rather than denying the contact or inferring a structural hair function for GATA1. Pair-specific natural isoform identity is not supplied by the gene-level table. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen records GATA1 interaction with CCDC24. Reason: The authentic HI-II-14 table and Q8N4L8-to-ORF crosswalk support the GATA1–CCDC24 pair. No more informative GATA1 activity is established by that contact in the inspected original material. Remove the nonspecific protein-binding label while retaining the positive yeast assay provenance and avoiding an invented regulatory or structural function. The library sequence and pair-specific isoform identity remain distinct. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: GATA1–FBF1 is a positive interaction, but bare protein binding is uninformative. Reason: Q8TES7 is directly identified as human FBF1 (GeneID 85302), and its retained UniProt record declares Q8TES7-6 and a GATA1 interaction. Original HI-II-14 Table S2G row 1874 independently records the positive GATA1–FBF1 gene pair. Remove the generic protein-binding annotation under the informativeness policy, preserving the positive assay and original accession suffix. Exact equivalence between isoform 6 and the pair-specific tested clone is not established, but that remaining limit does not make the partner gene unidentified or the interaction negative. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen supports a GATA1–RADIL contact. Reason: The original gene-level pair is RADIL. Retained later-library crosswalking links RADIL ORF54154 to Q96JH8-4, whereas this incoming annotation names Q96JH8 without a suffix; both literals are preserved and no per-pair isoform is invented. Remove the uninformative protein-binding annotation without rejecting the positive screen or assigning RADIL signaling functions to GATA1. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | MODIFY | Summary: GATA1 binds the transcriptional regulator HEXIM2 in the binary screen. Reason: GATA1 binds HEXIM2, a transcription coregulator identified as a PolII transcription inhibitor in the 7SK regulatory complex. GO:0001221 states binding to that partner class; it does not assert that GATA1 itself inhibits transcription or recruits 7SK. The original HI-II-14 pair and Q96MH2/ORF12696 crosswalk are positive. One discovery screen is distinct from the required individual quadruplicate retesting (at least 3/4 positive), autoactivation counterselection and sequence confirmation. No pair-specific orthogonal confirmation, physiological effect or natural-product assignment is inferred. Proposed replacements: transcription coregulator binding |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: The original binary screen records GATA1 interaction with KRTAP9-2. Reason: The selected original interaction table and Q9BYQ4/ORF53991 crosswalk support this positive gene pair. The screen does not establish an informative molecular function of GATA1 through the keratin-associated partner. Remove bare protein binding under specificity policy, retaining the positive experimental observation and its human-ORF-in-yeast context rather than inferring a tissue-level structural role. |
| GO:0005515 protein binding | IPI PMID:32911434 A functionally defined high-density NRF2 interactome reveals... | MODIFY | Summary: The original NRF2 screen directly records GATA1 as a positive binary partner. Reason: Supplementary Table S1 row 2 explicitly marks GATA1 positive in the targeted NRF2 yeast two-hybrid screen, and Table S2 records the GATA1 constructs. Selected original Methods require reproducible ADE2/HIS3 reporter responses in two independent assays after excluding autoactivation. Q16236 is the sequence-specific factor NRF2/NFE2L2, so transcription-factor binding is more informative than bare binding. Aggregate coIP, FCCS and DULIP results are not assigned to this pair without its individual result, and no oxidative-stress process is inferred for GATA1. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: file:human/GATA1/GATA1-external-evidence.md GATA1 | 2623 | C. elegans interolog, CCSB | Yes |
| GO:0005515 protein binding | IPI PMID:35512704 Systematic discovery of mutation-directed neo-protein-protei... | REMOVE | Summary: The original supplemental assays detect GATA1 contact with engineered SPOP-F133L. Reason: The authentic S3B table records positive GST pulldown in HEK293T and NanoPCA in HCT116 for SPOP-F133L–GATA1; a separate supplementary table reports positive NanoPCA in LNCaP C4-2 cells. Other listed assays are N/A, not negative. These positive mutant-partner assays do not establish a physiological wild-type SPOP interaction or a GATA1 ubiquitin-ligase activity. Remove the generic protein-binding label as uninformative while preserving the exact incoming O43791 record and the measured mutant context. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: The mouse ortholog transfer agrees with directly supported human cis-regulatory DNA binding. Reason: The literal P17679 ortholog transfer is consistent with human GATA1 binding erythroid promoter motifs and the ZNF268 upstream site. Current donor GOA contains an experimental DNA-binding record, while independent human assays establish the whole claim without assuming that the donor experiment used human protein. Preserve the incoming orthology and source fields. |
| GO:0000987 cis-regulatory region sequence-specific DNA binding | IEA GO_REF:0000107 | MODIFY | Summary: The conserved regulatory DNA-binding activity is specifically associated with PolII genes. Reason: Human gamma-globin and ZNF268 promoter experiments establish the polymerase context missing from this broader ortholog-derived label. GO:0000978 is a verified typed descendant of GO:0000987. Refine the term while retaining the literal mouse donor and original electronic provenance; no donor-species or source-error inference is needed. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0001221 transcription coregulator binding | IEA GO_REF:0000107 | ACCEPT | Summary: GATA1 directly binds transcriptional coregulators including FOG1. Reason: Human FOG1 interaction evidence and compensatory GATA1/FOG1 mutant experiments establish the partner role independently of the mouse ortholog transfer. FOG1 can support distinct activating and repressive GATA1 contexts, so coregulator binding is appropriately broader than coactivator-only binding. Preserve the original donor records rather than replacing them with the corroborating sources. |
| GO:0001223 transcription coactivator binding | IEA GO_REF:0000107 | ACCEPT | Summary: GATA1 binds coactivators that couple its regulatory DNA occupancy to transcription. Reason: The literal mouse ortholog transfer is consistent with the independently demonstrated human GATA1–MED1 interaction and the CCAR1/CoCoA recruitment route. MED1 binding and transcriptional coactivation are tested with appropriate domain and reporter comparisons; an indirect MED1(1–602) recruitment route is distinguished from direct GATA1 binding. This does not attribute the cofactors’ catalytic activities to GATA1. |
| GO:0001228 DNA-binding transcription activator activity, RNA polymerase II-specific | IEA GO_REF:0000107 | ACCEPT | Summary: GATA1 activates transcription of erythroid genes through sequence-specific DNA binding. Reason: Human promoter reporter and endogenous chromatin evidence supports the activating branch of GATA1 function, consistent with the mouse ortholog transfer. GATA1 also represses other loci, but that does not negate this experimentally supported activating activity. Preserve the donor/evidence fields and the separate negative-regulation contexts. |
| GO:0002039 p53 binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: GATA1 directly binds the p53 transactivation region in a context-dependent regulatory interaction. Reason: The literal electronic transfer is from mouse P17679 and remains unchanged. Selected original PMID:19411634 Methods/Results include purified human GATA1 fragments tested by GST binding and ITC, plus reciprocal native mouse MEL co-immunoprecipitation. Linker-plus-C-terminal-finger binding and DNA competition support the specific p53 interaction; separate mouse deletion experiments are not relabeled as human assays. This regulatory antagonism is supported but is less central than erythroid DNA recognition and lineage-cofactor recruitment. The discussion prediction about GATA1s is not an assay of that natural product. |
| GO:0003677 DNA binding | IEA GO_REF:0000120 | MODIFY | Summary: The conserved DNA-binding activity is specifically directed at PolII cis-regulatory motifs. Reason: Human gamma-globin promoter experiments and endogenous K562 ZNF268 occupancy establish sequence-specific regulatory DNA recognition. The generic electronic DNA-binding label is correct but lacks this established specificity. GO:0000978 is a verified descendant, so refine the term without changing the literal mouse/rat donor provenance or implying all donor experiments used human constructs. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0003682 chromatin binding | IEA GO_REF:0000120 | MODIFY | Summary: GATA1 binds chromatin DNA at regulated promoters. Reason: Endogenous K562 ChIP and sequence-specific binding to the ZNF268 upstream element establish the DNA-associated chromatin interaction, corroborated at gamma-globin regulatory sites. Refine the electronic chromatin-binding term to GO:0031490 chromatin DNA binding while preserving the ortholog/source fields. This is not an assertion that GATA1 modifies histones or that chromatin occupancy alone proves regulation of every nearby gene. Proposed replacements: chromatin DNA binding |
| GO:0007204 positive regulation of cytosolic calcium ion concentration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Gata1 transcriptional control can support antigen-evoked calcium mobilization in rat mast-cell models. Reason: The actual rat donor chain reaches IMP PMID:22390417. Its authentic abstract reports GATA1 and/or GATA2 knockdown in RBL-2H3 cells, reduced antigen-induced calcium mobilization and PLC-gamma1 expression, with promoter ChIP/reporter support for transcriptional control. The separately described mouse bone-marrow experiment concerns GATA2. Retain the human transfer as a context-dependent non-core role, not direct calcium-channel activity or a new human assay. |
| GO:0010559 regulation of glycoprotein biosynthetic process | IEA GO_REF:0000107 | UNDECIDED | Summary: The donor platelet phenotype does not yet resolve regulation of glycoprotein biosynthesis. Reason: The literal mouse transfer has genuine IMP PMID:15701726 grounding, alongside later human-derived propagation records. The authentic abstract reports reduced surface GPVI, especially in mouse-deficient platelets, and selective collagen responses. Full Methods and Results were not recovered, so synthesis cannot be separated from altered expression, trafficking or turnover. Preserve the electronic context and leave the biosynthesis-specific claim undecided; no circularity or experimental misattribution is alleged. |
| GO:0010724 regulation of definitive erythrocyte differentiation | IEA GO_REF:0000107 | ACCEPT | Summary: GATA1 regulates definitive erythroid differentiation through its transcriptional activity. Reason: The verified mouse donor chain reaches the original R216Q differentiation study, not only propagated annotations. Wild-type and engineered GATA1 activation in erythroid G1E models, interpreted alongside human disease evidence, support regulation of the definitive erythroid program. The human electronic transfer remains distinct from the murine construct assays and does not imply that every mutation abolishes differentiation. |
| GO:0031100 animal organ regeneration | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Rat liver GATA-related activation is evidence of a regenerative response, with a broader participation claim insufficiently resolved. Reason: Selected original PMID:18990226 Results, activation Methods and Discussion measure GATA1-associated DNA-binding activity in remnant-liver nuclear extracts and infer regulatory networks from enriched promoter motifs after partial hepatectomy. This is genuine rat evidence, not a PAINT phylogenetic analysis. It does not directly test a Gata1-specific contribution to organ regeneration or establish the broad transferred human process. Mark the process inference as over-annotated while preserving the positive response and leaving a possible regulatory role open. |
| GO:0043306 positive regulation of mast cell degranulation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Gata1 can enhance mast-cell degranulation indirectly through transcriptional control. Reason: The actual rat donor IMP PMID:22390417 reports decreased antigen-induced degranulation after GATA1 and/or GATA2 knockdown in RBL-2H3 cells, linked to PLC-gamma1 transcription. The separately reported mouse primary mast-cell result concerns GATA2, not an additional GATA1 experiment. Retain the specific human ortholog transfer as non-core, without assigning GATA1 a granule-fusion or calcium-channel molecular activity. |
| GO:0045893 positive regulation of DNA-templated transcription | IEA GO_REF:0000120 | MODIFY | Summary: GATA1 positively regulates transcription of PolII target genes. Reason: The electronic rule/ortholog assignment agrees with human globin promoter activation and coactivator recruitment. GO:0045944 is a verified descendant that supplies the established RNA polymerase II context. This positive annotation complements direct repression at other targets rather than asserting a universal activating effect. Proposed replacements: positive regulation of transcription by RNA polymerase II |
| GO:0060009 Sertoli cell development | IEA GO_REF:0000107 | UNDECIDED | Summary: The Sertoli-development transfer is not resolved by the accessible promoter study. Reason: The actual rat donor IEP PMID:9089398 examines testis-specific Gata1 promoter structure and expression, including rodent promoters and reporter regulation in cell lines. The accessible abstract does not expose a Gata1-dependent Sertoli-cell developmental assay, and expression or promoter regulation alone does not settle that process. Preserve the donor provenance and leave the human transfer undecided rather than treating the testis expression as false. |
| GO:0061629 RNA polymerase II-specific DNA-binding transcription factor binding | IEA GO_REF:0000107 | ACCEPT | Summary: The conserved GATA1–PU.1 interaction is transcription-factor binding. Reason: The actual electronic source chain reaches mouse Gata1/P17679 IPI PMID:18063754 with PU.1/P17433. Selected original co-immunoprecipitation and ETS-reporter experiments test this interaction and its disruption by FOG1; the official PU.1 identity is a DNA-binding transcription factor. Preserve the human electronic transfer, rather than treating the 293T host as proof of a human GATA1 construct. This is informative partner-role binding and does not assert a purified binary assay or a new developmental process. |
| GO:0070527 platelet aggregation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: The ortholog evidence supports a context-dependent platelet aggregation phenotype. Reason: The actual mouse donor chain includes IMP PMID:15701726, in which the authentic abstract reports impaired collagen-induced aggregation in Gata1-deficient mice and a human R216Q patient, with GPCR agonist responses preserved. Retain this downstream platelet-functional role as non-core. GATA1’s transcriptional programming is not described as a direct platelet–platelet adhesion molecule, and the current donor’s propagated rows are not mistaken for the sole evidence. |
| GO:0071222 cellular response to lipopolysaccharide | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: GATA-factor promoter occupancy accompanies an LPS-responsive cytokine program in rat mast cells. Reason: LPS-induced GATA occupancy at the IL5 promoter and cytokine output provide functional context beyond an expression change. The authentic PMID:17687519 abstract reports ChIP, IL5/IL13 RNA and secreted protein in rat RBL-2H3 cells, with thymoquinone-sensitive GATA expression and promoter binding. Retain the curator-backed rat-to-human response annotation as non-core. The abstract does not resolve individual GATA1-versus-GATA2 antibody specificity or a GATA1-specific perturbation, so no exclusive human mechanism is added. |
| GO:0071320 cellular response to cAMP | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: cAMP regulates GATA1 abundance and reported DNA binding, without resolving its participation in the stimulus response. Reason: Selected original PMID:11861504 Results show cAMP suppressing Gata1 RNA/protein in mouse MA-10 cells, with reduced INHA-motif EMSA binding reported as data not shown; MEL cells differ. Discussion cites an earlier study in which GATA-site mutations reduced basal promoter activity without affecting cAMP stimulation, and leaves GATA1–CREB competition unresolved. These positive responses of GATA1 do not establish a GATA1-mediated stimulus-response step. Mark this human participation inference as over-annotated while preserving the rat IEP donor provenance and leaving a possible regulatory role open. |
| GO:0071372 cellular response to follicle-stimulating hormone stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: FSH suppression of Gata1 in rat Sertoli cells does not by itself establish a GATA1-mediated FSH response. Reason: Selected original PMID:11861504 shows FSH-dependent reduction of Gata1 RNA in primary Sertoli cultures from 21-day-old rats. The associated cAMP work retains positive abundance and reported DNA-binding effects, but an identified GATA1-dependent stimulus-response mechanism remains unresolved. Mark the source-specific human participation inference as over-annotated rather than rejecting the observed response. The separate Sertoli-development uncertainty derives from PMID:9089398, not this experiment. |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: The HPA nucleoplasm annotation fits GATA1’s nuclear transcriptional function. Reason: Retain the original HPA immunofluorescence-based localization assertion. Independent human chromatin-occupancy and nuclear-binding experiments strongly support nucleoplasmic GATA1; no new claim is made about particular antibody images, cell lines or exclusive localization that were not inspected here. The more specific nuclear compartment is compatible with the separately retained nucleus terms. |
| GO:0005634 nucleus | EXP PMID:35030251 Congenital anemia reveals distinct targeting mechanisms for ... | ACCEPT | Summary: The R307C/H study directly tests GATA1 nuclear localization. Reason: Selected original Methods and Figure 4 caption/Results compare nuclear and cytoplasmic fractions in G1E cells expressing wild-type or mutant GATA1, with LaminB and GAPDH purity controls. The mutants show reduced nuclear abundance, not complete absence of nuclear GATA1. Patient-derived human erythroid observations and the engineered G1E/ER models remain distinct, and the latter are not natural splice products. Supporting Evidence: |
| GO:0001221 transcription coregulator binding | IPI PMID:12483298 Molecular cloning and characterization of the GATA1 cofactor... | ACCEPT | Summary: GATA1 binds the transcriptional coregulator FOG1/ZFPM1. Reason: The incoming partner Q8IX07 is FOG1. The source clones human FOG1 and tests the effects of GATA1 zinc-finger substitutions on the interaction, with human/mouse FOG1 differences explicitly considered. This directly informs recruitment of a transcriptional coregulator rather than generic protein binding. The authentic abstract was read; detailed original assay images were not recovered in this packet. Independent original human GATA1/FOG1 interaction experiments corroborate the claim. |
| GO:1990837 sequence-specific double-stranded DNA binding | IDA PMID:28473536 Impact of cytosine methylation on DNA binding specificities ... | MODIFY | Summary: The high-throughput DNA-binding assertion is consistent with the independently established promoter specificity. Reason: The retained original supplementary workbook directly records GATA1 eDBD sequence-specific DNA-binding models from methyl-HT-SELEX and HT-SELEX (Table S1 row 293; Table S2 rows 8218 and 8223). Although S1 also lists a full-length sequence, these two positive models explicitly use eDBD; no natural-product-specific methylation response is inferred. Separate direct human gamma-globin and ZNF268 promoter experiments support the more specific GO:0000978 function. The RNA polymerase II and cis-regulatory interpretation comes from those promoter experiments, rather than from random-library selection alone. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0005515 protein binding | IPI PMID:17167422 Hsp70 regulates erythropoiesis by preventing caspase-3-media... | REMOVE | Summary: The recorded GATA1–caspase-3 contact is a substrate-cleavage relationship. Reason: The literal partner is CASP3/P42574, not Hsp70. Selected original supplemental Methods and primary figure captions establish reconstructed caspase-3 cleavage of GATA1 and an engineered cleavage-site mutant, with Hsp70-depletion rescue distinguished from erythropoietin-withdrawal observations. This is positive biochemical contact, but the bare protein-binding label does not identify a useful GATA1 molecular function. Remove that uninformative annotation under binding policy without denying cleavage, changing the preserved part_of GO:0043065 atom, or assigning protease activity to the substrate. Supporting Evidence: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:2467208 Increased gamma-globin expression in a nondeletion HPFH medi... | ACCEPT | Summary: The original human gamma-globin experiments support positive promoter regulation by GATA1. Reason: The authentic PMID:2467208 abstract links the GF-1/GATA binding sites and an HPFH regulatory mutation to erythroid-specific promoter output. This supports positive regulation of a PolII gene, corroborated by later direct GATA1/coactivator experiments. The historical extract is not assigned to a specific current natural product without sequence evidence. |
| GO:0000785 chromatin | ISA GO_REF:0000113 | ACCEPT | Summary: GATA1 associates with regulatory chromatin. Reason: The TFclass structural assignment is consistent with original human K562 chromatin immunoprecipitation at ZNF268 and gamma-globin regulatory regions. Chromatin is an appropriate location for the DNA-bound transcription factor. This does not imply uniform occupancy of all chromatin or histone-modifying catalysis by GATA1. |
| GO:0000981 DNA-binding transcription factor activity, RNA polymerase II-specific | ISA GO_REF:0000113 | ACCEPT | Summary: TFClass assignment agrees with GATA1 acting as a sequence-specific PolII transcription factor. Reason: The classification is supported by direct GATA1 promoter recognition, reporter activity and endogenous chromatin occupancy. This is a DNA-binding regulatory activity, not merely recruitment as a non-DNA-binding cofactor. Both activating and repressive outputs make the unpolarized PolII transcription-factor term informative. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: GATA1 binds regulatory DNA while recruiting distinct activating and repressive complexes. Reason: Selected original ChIP, DNA-binding and recruitment experiments support sequence-specific promoter occupancy. The tagged GATA1 provenance is murine through the cited construct paper; human regulatory DNA and HeLa recipients do not establish a human coding sequence. This conserved mechanism agrees with independent human GATA1 occupancy. The study resolves separate FOG1, TAL1/LDB1, GFI1B and remodeling complexes, rather than one supercomplex. |
| GO:0001228 DNA-binding transcription activator activity, RNA polymerase II-specific | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: GATA1 supplies sequence recognition and activation within erythroid transcriptional complexes. Reason: The original selected activation/recruitment experiments and G1E comparisons establish the conserved regulatory mechanism. Murine tagged constructs and heterogeneous host cells are explicitly distinguished from direct human protein assays, while independent human promoter experiments corroborate the whole claim. Do not infer that every isolated GATA1 complex is activating: separate FOG1-dependent repression and other complexes are also described. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: Distinct GATA1 cofactor complexes support transcriptional activation. Reason: The original complex study identifies activating TAL1/LDB1-associated GATA1 assemblies as well as separate repressive complexes. Retain positive PolII regulation without collapsing these complexes or making all their catalytic functions GATA1 activities. Construct provenance remains murine for the tagged GATA1 preparation, with independent human promoter studies corroborating the function. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IMP PMID:20133935 Developmental silencing of human zeta-globin gene expression... | ACCEPT | Summary: GATA1 occupies the activating portion of the human zeta-globin ZF2 element. Reason: The original K562/MEL EMSA, competition and anti-GATA1 supershift distinguish the GATA1 complex from RREB1 complexes. Mutation of the GATA1 site reduces promoter output, whereas mutation of the adjacent RREB1 site derepresses it. The title foregrounds RREB1 but the paper directly tests GATA1 recognition. Preserve the erythroid-cell and transcript input extensions; the additional RREB1 knockdown assays do not become GATA1 knockdown evidence. Supporting Evidence: |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IDA PMID:24245781 CCAR1/CoCoA pair-mediated recruitment of the Mediator define... | ACCEPT | Summary: Endogenous GATA1 binds the gamma-globin promoter and recruits transcriptional cofactors. Reason: K562 ChIP places GATA1 at the gamma-globin cis-regulatory sites; GATA1 knockdown reduces cofactor recruitment. The original also uses separately identified mouse and human engineered proteins for interaction assays. Endogenous human chromatin occupancy supports the present DNA-binding claim, without assuming every recombinant construct is human or that GATA1 itself catalyses chromatin modification. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:26019275 A Novel In-Frame Deletion in the Leucine Zipper Domain of C/... | MODIFY | Summary: The CEBPE study supports GATA1 association with other hematopoietic DNA-binding transcription factors. Reason: The authentic PMID:26019275 abstract explicitly compares a CEBPE leucine-zipper deletion with wild type and reports impaired association with GATA1 and PU.1, alongside altered cooperative transcription. The incoming connected partner set P17947/Q15744 is retained as a set, not split into invented independent experiments. Both verified partners are DNA-binding transcription factors, supporting GO:0061629. Exact original construct species and separate ternary-versus-binary assay configuration remain unverified because the full Methods were inaccessible. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0003677 DNA binding | IDA PMID:12609092 A novel erythroid differentiation related gene EDRF1 upregul... | MODIFY | Summary: The HEL-cell study directly monitors GATA1 regulatory DNA-binding activity. Reason: The authentic PMID:12609092 abstract explicitly reports EMSA of GATA1 and NF-E2 in human HEL cells after EDRF1 sense/antisense expression. Thus the EDRF1-focused title does not make this a wrong-gene citation. The detailed probe and gel were not recovered here; independent direct human GATA1 promoter experiments establish the more informative GO:0000978 specificity. Keep that access limit and the original IDA source while refining the broad term. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0032993 protein-DNA complex | IDA PMID:12609092 A novel erythroid differentiation related gene EDRF1 upregul... | ACCEPT | Summary: GATA1 forms a protein–DNA complex in the HEL-cell binding assay. Reason: The authentic PMID:12609092 abstract explicitly reports EMSA measurements of GATA1 DNA-binding activity in human HEL cells. That supports the protein–DNA complex assertion despite the paper’s EDRF1 focus; the detailed original gel was not recovered. Independent human promoter binding and chromatin occupancy support the same central physical role, without inventing the precise gel complex composition. |
| GO:0005515 protein binding | IPI PMID:24245781 CCAR1/CoCoA pair-mediated recruitment of the Mediator define... | MODIFY | Summary: GATA1 binds MED1 and recruits coactivators to the gamma-globin promoter. Reason: Selected original PMID:24245781 biochemical interaction, domain comparisons, K562 ChIP and cofactor-depletion assays support MED1 recruitment and transcriptional coactivation. The direct GATA1–MED1 interaction is distinguished from CCAR1/CoCoA-assisted recruitment of MED1(1–602). Human and mouse constructs are separately described in the source. GO:0001223 supplies the informative coactivator-binding activity without treating every Mediator association as an independent direct contact. Proposed replacements: transcription coactivator binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:24245781 CCAR1/CoCoA pair-mediated recruitment of the Mediator define... | MODIFY | Summary: GATA1 binds the CCAR1 transcriptional coactivator. Reason: Q8IX12 is CCAR1, verified in the official human record. Original PMID:24245781 interaction assays and functional coactivation/knockdown experiments place CCAR1 with CoCoA in GATA1-driven gamma-globin activation. This supports transcription coactivator binding. CCAR1-assisted recruitment of MED1 fragments is an indirect route and is not confused with direct binding of every component, nor does the result establish all CCAR1 functions as GATA1 functions. Proposed replacements: transcription coactivator binding Supporting Evidence: PMID:24245781 GATA1 directly interacts with CCAR1 in vitro |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:24245781 CCAR1/CoCoA pair-mediated recruitment of the Mediator define... | MODIFY | Summary: The gamma-globin coactivator study supports positive PolII transcriptional regulation. Reason: Selected original PMID:24245781 reporter, binding, ChIP and cofactor-depletion experiments concern GATA1-driven gamma-globin transcription. Refine the generic DNA-templated-transcription regulation term to GO:0045944, retaining the source and distinguishing direct GATA1–MED1 association from CCAR1/CoCoA-assisted recruitment. This is a verified descendant refinement, not an additional process assertion. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IMP PMID:20133935 Developmental silencing of human zeta-globin gene expression... | ACCEPT | Summary: GATA1 positively regulates the zeta-globin promoter in the erythroid context. Reason: Selected original PMID:20133935 reporter mutations and GATA1-binding assays distinguish the positive GATA element from a repressive RREB1 element. The RREB1 knockdown experiment is not relabeled as GATA1 depletion. Preserve the literal erythrocyte and ENST00000252951 extension atoms; the observed GATA-dependent promoter response supports positive PolII transcriptional regulation. Supporting Evidence: |
| GO:0005634 nucleus | IDA PMID:17167422 Hsp70 regulates erythropoiesis by preventing caspase-3-media... | ACCEPT | Summary: Nuclear GATA1 is protected during erythroid differentiation. Reason: Selected primary figure captions and supplemental Methods describe GATA1 in human erythroid nuclei and its protection from caspase-mediated cleavage in the Hsp70 context. Preserve the existence_overlaps erythrocyte-differentiation extension exactly. Nuclear localization is supported independently of any stronger claim about an apoptotic signaling subtype or direct Hsp70 binding in a different annotation. Supporting Evidence: |
| GO:0000122 negative regulation of transcription by RNA polymerase II | IDA PMID:22235304 Knockdown of ZNF268, which is transcriptionally downregulate... | ACCEPT | Summary: GATA1 directly represses the ZNF268 promoter in K562 cells. Reason: Selected original competition/supershift, promoter mutation, ChIP and GATA1 perturbation experiments support sequence-specific repression of ZNF268 transcription. This directly fits negative regulation of PolII transcription. Later phenotypes caused by ZNF268 knockdown are not used as additional GATA1 process evidence. Supporting Evidence: |
| GO:0003677 DNA binding | IDA PMID:22235304 Knockdown of ZNF268, which is transcriptionally downregulate... | MODIFY | Summary: GATA1 recognizes a defined upstream regulatory site of human ZNF268. Reason: The original K562 study tests the G1 site by competition, anti-GATA1 supershift, mutated reporters and ChIP. These experiments distinguish sequence-specific regulatory binding from generic DNA association and support GO:0000978. Later phenotypes after ZNF268 knockdown are not GATA1 perturbation experiments and are not used to create additional processes. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding Supporting Evidence: PMID:22235304 GATA-1 binds directly to the G1 binding site |
| GO:0031490 chromatin DNA binding | IDA PMID:22235304 Knockdown of ZNF268, which is transcriptionally downregulate... | ACCEPT | Summary: GATA1 occupies chromatin DNA at the ZNF268 regulatory region. Reason: Original K562 chromatin immunoprecipitation, motif-directed binding and reporter experiments establish binding to DNA assembled in chromatin. GO:0031490 accurately captures that aspect. The sequence-specific PolII cis-regulatory term used elsewhere is not a verified descendant of this chromatin-DNA term, so the distinct chromatin context is retained rather than replaced by a falsely claimed refinement. Supporting Evidence: |
| GO:2001240 negative regulation of extrinsic apoptotic signaling pathway in absence of ligand | IMP PMID:17167422 Hsp70 regulates erythropoiesis by preventing caspase-3-media... | UNDECIDED | Summary: The precise ligand-absence extrinsic-apoptosis subtype is not established by the inspected rescue experiment. Reason: Selected primary PMID:17167422 materials distinguish erythropoietin-withdrawal observations from the caspase-resistant GATA1 rescue after Hsp70 depletion performed with Epo and IL3 present. The latter supports a survival role but cannot by itself establish this narrowly specified absence-of-ligand extrinsic signaling process. Because the complete main Results remain inaccessible, preserve the original IMP assertion as undecided rather than claiming a whole-paper contradiction; the broader anti-apoptotic annotation is assessed separately. Supporting Evidence: |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8935740 | ACCEPT | Summary: Reactome places GATA1 in the ITGA2B promoter-associated regulatory assembly. Reason: The retained normal reaction explicitly recruits the GATA1–ZFPM1 complex to the ITGA2B promoter with RUNX1-associated factors. This is consistent with nucleoplasmic GATA1 and independent nuclear evidence. Proposed recruitment routes and the activities of PRMT1, MLL, EP300 and KAT2B remain attributed to those proteins, not to GATA1. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8936481 | ACCEPT | Summary: GATA1 is represented in the nuclear ITGA2B chromatin context of the MLL reaction. Reason: The retained reaction describes MLL-mediated H3K4 methylation at the ITGA2B promoter, with recruitment through RUNX1 and possibly GATA1. The location assertion is supported by that promoter-associated context and independent nuclear evidence; it does not assign methyltransferase activity to GATA1 or strengthen the source’s qualified recruitment mechanism. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8936616 | ACCEPT | Summary: Reactome includes GATA1–ZFPM1 at the GP1BA promoter. Reason: The normal event explicitly describes the GATA1 coregulator complex at the platelet glycoprotein Ib alpha promoter. The nucleoplasmic location is appropriate for this transcriptional assembly. Keep the source’s analogy-based PRMT1 effect distinct from directly established GATA1 occupancy, and do not make all recruited chromatin-enzyme reactions GATA1 activities. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8936621 | ACCEPT | Summary: The GP1BA MLL event retains GATA1’s nuclear promoter context. Reason: This is a histone methylation event performed by the MLL complex; the source qualifies recruitment via RUNX1 and possibly GATA1. Retain nucleoplasm for the associated GATA1 transcriptional component, corroborated by independent nuclear evidence, without interpreting event membership as GATA1 histone-methylating catalysis. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8936979 | ACCEPT | Summary: Reactome recruits GATA1–ZFPM1 to the THBS1 regulatory region. Reason: The retained event explicitly names GATA1 within the THBS1 promoter-associated assembly. Nucleoplasm is consistent with that transcriptional context. The summary’s assumed pre-existing H3K4me2 mark and analogy-based PRMT1 effect remain qualified; no direct GATA1 methyltransferase or acetyltransferase role follows from the complex. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8937016 | ACCEPT | Summary: The THBS1 chromatin-modification event supports a nuclear regulatory context. Reason: The source explicitly marks MLL methylation of the THBS1 nucleosome as an assumed event based on chromatin and transcription observations. Its GATA1 component is a transcriptional participant in that nuclear context, not the catalytic methyltransferase. Retain the location with independent GATA1 nuclear evidence while preserving the source’s inferential limits. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8937037 | ACCEPT | Summary: Reactome includes GATA1–ZFPM1 at the MIR27A promoter. Reason: The retained normal event explicitly recruits the GATA1 cofactor complex with RUNX1 and other chromatin-associated factors at MIR27A. Nucleoplasmic location is supported. The annotation is not expanded into a microRNA-processing activity or into all enzymatic functions of the recruited histone regulators. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8937050 | ACCEPT | Summary: The MIR27A MLL event retains GATA1 within a nuclear promoter assembly. Reason: The source describes MLL-dependent H3K4 methylation, with recruitment through RUNX1 and possibly GATA1. This supports the location of the associated transcription factor while leaving the methyl transfer assigned to MLL. Independent human GATA1 chromatin evidence supports nucleoplasm without making the qualified recruitment route certain. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-8956568 | ACCEPT | Summary: The official Reactome participant chain explicitly includes nucleoplasmic GATA1. Reason: The event input R-HSA-8956524 contains the GATA-factor set R-HSA-8956530, whose actual member R-HSA-996772 identifies human P15976 chain 1–413 in the nucleoplasm. This is verified curated-model membership, not a claim that each cited experiment tested every alternative GATA combination. The common set’s GATA2 member is kept distinct. Supporting Evidence: Reactome:R-HSA-8956568 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-996755 | ACCEPT | Summary: The official Reactome GATA-factor set includes the exact human GATA1 entity. Reason: The event input set R-HSA-996770 has member R-HSA-996772, explicitly human P15976 chain 1–413 and nucleoplasmic. The verified participant chain supports the location assertion. It does not imply that all paralog combinations represented by the set were assayed together or that GATA1 gains another component’s catalytic function. Supporting Evidence: Reactome:R-HSA-996755 |
| GO:0043066 negative regulation of apoptotic process | IMP PMID:17167422 Hsp70 regulates erythropoiesis by preventing caspase-3-media... | KEEP AS NON CORE | Summary: Preserved GATA1 contributes to erythroid-cell survival in the Hsp70/caspase context. Reason: Selected original PMID:17167422 supplemental Methods and primary captions link GATA1 cleavage to survival and differentiation, with an engineered caspase-resistant mutant supporting rescue after Hsp70 depletion. The broader anti-apoptotic effect is supported within this erythroid context and is non-core relative to GATA1’s transcriptional and lineage functions. Preserve the occurs_in nucleus atom; do not equate the rescue performed with Epo/IL3 present to a specific ligand-withdrawal experiment. |
| GO:0045648 positive regulation of erythrocyte differentiation | IMP PMID:17167422 Hsp70 regulates erythropoiesis by preventing caspase-3-media... | ACCEPT | Summary: GATA1 promotes erythroid differentiation when protected from cleavage. Reason: Selected original PMID:17167422 supplemental Methods and figure captions establish a GATA1-dependent erythroid outcome and engineered cleavage-site rescue after Hsp70 depletion. This agrees with independent GATA1 differentiation studies. Preserve the original nuclear extension and distinguish the Hsp70-depletion rescue conditions from separate erythropoietin-withdrawal observations. |
| GO:0005667 transcription regulator complex | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: GATA1 participates in distinct transcription-regulatory complexes. Reason: Selected original PMID:15920471 Results and Methods identify separate TAL1/LDB1, FOG1/MeCP1, GFI1B and ACF/WCRF assemblies associated with tagged GATA1. The tagged construct is traced to murine GATA1, with distinct human erythroid evidence corroborating the conserved regulatory role. The broad complex term accommodates several experimentally separated assemblies; it does not collapse them into a single supercomplex. |
| GO:0010724 regulation of definitive erythrocyte differentiation | IDA PMID:12200364 X-linked thrombocytopenia with thalassemia from a mutation i... | ACCEPT | Summary: The R216Q study tests GATA1-driven erythroid differentiation. Reason: Selected original PMID:12200364 Results show GATA1-dependent maturation in the G1E model while distinguishing DNA-face and FOG-face defects. R216Q retains considerable differentiation activity; the modest reported difference is not presented as a categorical loss or a statistically definitive defect, and the human globin imbalance is not fully reproduced by the model. The demonstrated GATA1 regulatory role supports this process. Supporting Evidence: |
| GO:0010724 regulation of definitive erythrocyte differentiation | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: GATA1 regulatory complexes contribute to definitive erythroid differentiation. Reason: The original complex study relates distinct activating and repressing GATA1 assemblies to erythroid differentiation programs. The tagged GATA1 construct is traced to murine origin, and the complexes are not combined into one supercomplex. Independent GATA1 differentiation experiments corroborate the conserved direct transcriptional role underlying this process, without assigning the enzymatic functions of recruited chromatin regulators to GATA1. |
| GO:0017053 transcription repressor complex | IDA PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | ACCEPT | Summary: GATA1 is part of transcription-repressing assemblies. Reason: The original complex study distinguishes repressive GATA1 associations, including FOG1 bridging to MeCP1 and other separate complexes, from activating TAL1/LDB1 assemblies. This supports transcription repressor complex membership while preserving the construct provenance and the distinction between direct binding and co-complex association. Independent human ZNF268 repression corroborates a repressive GATA1 function. |
| GO:0030220 platelet formation | IMP PMID:11675338 X-linked thrombocytopenia caused by a novel mutation of GATA... | ACCEPT | Summary: The G208S cofactor-binding defect supports GATA1’s platelet-formation role. Reason: The authentic PMID:11675338 abstract describes a GATA1 N-finger mutation with macrothrombocytopenia and partially disrupted FOG interaction. Independent human GATA1 variant studies corroborate the same transcriptional pathway. Retain platelet formation while distinguishing the positive clinical/cofactor evidence from detailed original assay images not inspected here. Supporting Evidence: PMID:11675338 the GATA-1-FOG interaction is partially disrupted |
| GO:0030220 platelet formation | IMP PMID:12483298 Molecular cloning and characterization of the GATA1 cofactor... | ACCEPT | Summary: Human GATA1–FOG1 interaction defects support platelet development. Reason: The original publisher abstract for PMID:12483298 explicitly reports disturbed GATA1–FOG1 interaction in patient platelets and erythrocytes carrying D218 substitutions, in a macrothrombocytopenia context. Together with independent GATA1 disease evidence, this supports the central platelet-formation role. It does not resolve the separate precise zinc-finger-class assertion or imply that all natural products were tested. |
| GO:0035854 eosinophil fate commitment | IDA PMID:12045236 Essential and instructive roles of GATA factors in eosinophi... | ACCEPT | Summary: GATA1 promotes commitment to the eosinophil lineage. Reason: The selected original PMID:12045236 main text describes increased eosinophil colony output after GATA1 expression in human CD34-positive progenitors and impaired/rescued eosinophil development in the mouse system. These functional experiments support lineage commitment beyond expression correlation. The mouse GATA1 cDNAs and engineered deletions are not relabeled as natural human splice products. Supporting Evidence: |
| GO:0043565 sequence-specific DNA binding | IMP PMID:12200364 X-linked thrombocytopenia with thalassemia from a mutation i... | MODIFY | Summary: The R216Q study resolves sequence-specific recognition of a palindromic GATA regulatory site. Reason: Selected original PMID:12200364 Methods and Results compare the palindromic versus single GATA motif and distinguish defective DNA recognition from preserved FOG binding. Recombinant murine constructs and human clinical observations are separate evidence streams. Independent human promoter experiments supply the explicit PolII cis-regulatory context, supporting refinement to GO:0000978 without claiming the study assayed every natural human product. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:12200364 X-linked thrombocytopenia with thalassemia from a mutation i... | ACCEPT | Summary: GATA1 DNA recognition can activate PolII-regulated erythroid genes. Reason: The R216Q study distinguishes regulatory DNA recognition from FOG interaction and tests GATA1 function in an engineered erythroid model. Human clinical observations, murine recombinant proteins and the GATA1–ER model remain distinct. Positive transcriptional regulation is supported without claiming that the modest differentiation comparison proves complete loss of activation in R216Q. |
| GO:0061629 RNA polymerase II-specific DNA-binding transcription factor binding | IPI PMID:11675338 X-linked thrombocytopenia caused by a novel mutation of GATA... | MODIFY | Summary: The G208S study concerns binding to the FOG1 transcriptional coregulator. Reason: The incoming Q8IX07 partner is FOG1/ZFPM1. The authentic source abstract reports disrupted GATA1–FOG association, especially at FOG finger 9. FOG1 is a transcriptional coregulator, not established here as a sequence-specific DNA-binding PolII factor. Replace the partner-role term with GO:0001221 while retaining the literal source, partner and assay access limit; this correction is about the bound protein, not GATA1’s own DNA-binding identity. Proposed replacements: transcription coregulator binding |
| GO:0061629 RNA polymerase II-specific DNA-binding transcription factor binding | IPI PMID:15920471 GATA-1 forms distinct activating and repressive complexes in... | MODIFY | Summary: The complex study supports GATA1 binding to FOG1 as a coregulator. Reason: Selected original PMID:15920471 Results and Methods distinguish FOG1-containing complexes from TAL1/LDB1, GFI1B and ACF/WCRF assemblies, with FOG1 bridging GATA1 to MeCP1. The tagged GATA1 construct is traced to an explicitly murine construct despite the human beta-globin expression cassette. Q8IX07 denotes the FOG1 coregulator, so GO:0001221 is the appropriate partner-role correction; no direct DNA-binding activity of FOG1 or single combined supercomplex is inferred. Proposed replacements: transcription coregulator binding |
| GO:0000976 transcription cis-regulatory region binding | IMP PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | MODIFY | Summary: GATA1 recognizes sequence-specific cis-regulatory DNA at RNA polymerase II genes. Reason: The original V205M study separates loss of FOG1 recruitment from retained DNA recognition: WT and mutant GATA1 bind the tested erythroid regulatory sequence, while C204R is a DNA-binding control. The experimental Gata1 constructs are murine despite some human recipient cells. Independent human gamma-globin and ZNF268 assays establish the conserved PolII cis-regulatory sequence-specific activity. GO:0000978 is an actual typed descendant of this broader regulatory-region term; refine specificity without altering the incoming source or construct scope. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0000977 RNA polymerase II transcription regulatory region sequence-specific DNA binding | IDA PMID:2467208 Increased gamma-globin expression in a nondeletion HPFH medi... | MODIFY | Summary: Human GATA1 binds a defined gamma-globin cis-regulatory motif. Reason: The original human erythroleukemia nuclear-factor study identifies sequence-specific binding to the gamma-globin regulatory region and functional reporter effects. The more explicit PolII cis-regulatory sequence-specific term GO:0000978 is a verified descendant of GO:0000977 and describes this activity. The broader original identifier and evidence provenance are retained. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding Supporting Evidence: PMID:2467208 This effect is mediated by GF-1 |
| GO:0003677 DNA binding | IDA PMID:11418466 Platelet characteristics in patients with X-linked macrothro... | MODIFY | Summary: GATA1 DNA recognition persists despite a disease-associated FOG1-binding defect. Reason: Selected original PMID:11418466 assays distinguish the D218G cofactor defect from preserved binding to regulatory DNA. The sequence origin of the probe does not establish the protein construct species. Independent human promoter and chromatin assays establish the PolII cis-regulatory sequence-specific function represented by GO:0000978, a verified descendant of DNA binding. This specificity refinement neither converts the mutant into a natural splice product nor alleges an error in the original assay. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0003700 DNA-binding transcription factor activity | IDA PMID:2467208 Increased gamma-globin expression in a nondeletion HPFH medi... | MODIFY | Summary: The human gamma-globin study couples GATA1 motif recognition to promoter output. Reason: The authentic original abstract describes human erythroleukemia nuclear GF-1 binding to the gamma-globin regulatory motifs and the erythroid-specific promoter effect of the HPFH mutation. This supports DNA-dependent regulation of a PolII gene, with GO:0000981 providing a verified descendant of the broad transcription-factor term. The historical factor naming and original IDA fields are retained. Proposed replacements: DNA-binding transcription factor activity, RNA polymerase II-specific Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:11418466 Platelet characteristics in patients with X-linked macrothro... | MODIFY | Summary: The GATA1 interaction recruits the transcriptional coregulator FOG1. Reason: The incoming partner O35615 is explicitly mouse Zfpm1/FOG1, confirmed in the official record. The D218G study tests a weakened GATA1–FOG interaction while retaining DNA binding; human recipient cells or DNA probes do not identify the GATA1 construct species. Coregulator binding captures the supported partner role more informatively than bare protein binding. Independent human FOG1 and GATA1 interaction studies corroborate the conserved role without replacing the literal original partner. Proposed replacements: transcription coregulator binding |
| GO:0005634 nucleus | IDA PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | ACCEPT | Summary: The V205M study supports nuclear GATA1 in its experimental context. Reason: Selected original experiments distinguish localization and preserved DNA recognition from impaired FOG binding. The GATA1 constructs are mouse-derived; human cells used as recipients do not change their origin. This conserved localization is independently corroborated by human GATA1 nuclear and chromatin evidence, so retain the original nucleus assertion with accurate construct scope. |
| GO:0005634 nucleus | IDA PMID:2467208 Increased gamma-globin expression in a nondeletion HPFH medi... | ACCEPT | Summary: Human erythroleukemia nuclear extracts contain the GATA-binding factor. Reason: The authentic original PMID:2467208 abstract explicitly places the historical GF-1/GATA factor in human erythroleukemia nuclear extracts and tests gamma-globin regulatory DNA binding. This supports nucleus localization, corroborated by later direct GATA1 studies. No modern splice-product identity is assigned retrospectively to the historical extract. |
| GO:0008584 male gonad development | IMP PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | UNDECIDED | Summary: The male-gonad attribution remains uncertain in the original disease report. Reason: Selected original PMID:10700180 Discussion explicitly states that the relationship of cryptorchidism to the GATA1 mutation is unclear and may be unrelated, with normal testicular tissue noted. The convincing hematopoietic and cofactor experiments do not resolve this separate developmental claim. Preserve the original IMP assertion as undecided rather than treating the reported association as established causation or asserting that GATA1 has no gonadal role. Supporting Evidence: |
| GO:0010559 regulation of glycoprotein biosynthetic process | IMP PMID:15701726 Selective impairment of platelet activation to collagen in t... | UNDECIDED | Summary: The human and mouse platelet study establishes altered GPVI-associated function, with biosynthesis specificity unresolved. Reason: PMID:15701726 directly compares a human R216Q patient and Gata1-deficient mice. The available original abstract supports selective collagen/GPVI defects, but it does not expose a glycoprotein-synthesis, mRNA, promoter or turnover assay. Surface abundance alone does not identify the underlying mechanism. Retain the original IMP assertion as undecided pending the relevant full assay rather than removing a curator’s unseen experimental evidence. Supporting Evidence: |
| GO:0030218 erythrocyte differentiation | IEP PMID:7678994 Expression of tal-1 and GATA-binding proteins during human h... | ACCEPT | Summary: GATA1 participates in erythrocyte differentiation, beyond the original expression-pattern evidence. Reason: The original IEP study reports GATA1 expression in purified human erythroblasts and committed progenitors, with changes during terminal maturation. Its evidence code is preserved; expression alone is not relabeled as a perturbation assay. Independent direct differentiation and human disease studies establish GATA1’s transcriptional participation in the erythroid program. |
| GO:0030219 megakaryocyte differentiation | IMP PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | ACCEPT | Summary: GATA1–FOG disruption impairs the megakaryocytic differentiation program. Reason: The original V205M study combines a human hematopoietic phenotype with impaired GATA1–FOG binding and conserved differentiation experiments. This supports a central megakaryocytic regulatory role, distinct from the paper’s uncertain gonadal association. The preserved DNA binding does not imply intact cofactor-dependent lineage regulation. |
| GO:0030220 platelet formation | IMP PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | ACCEPT | Summary: GATA1 is required for the transcriptional program that produces functional platelets. Reason: The V205M disease study connects GATA1 cofactor dysfunction to thrombocytopenia and abnormal megakaryocytic development. Together with independent human FOG-binding variants, it supports platelet formation as a central lineage outcome of GATA1’s regulatory work. This does not assign a mechanical platelet-budding enzyme activity to the transcription factor. |
| GO:0030221 basophil differentiation | IEP PMID:7678994 Expression of tal-1 and GATA-binding proteins during human h... | UNDECIDED | Summary: The basophil differentiation assertion is not resolved by the accessible expression study. Reason: PMID:7678994 reports GATA1/tal-1 coexpression in purified human basophilic cells and suggests lineage regulation. That genuine IEP evidence is preserved, but the accessible abstract does not expose a direct GATA1-dependent basophil differentiation assay. The later mast-cell and eosinophil experiments are not interchangeable with basophil differentiation. Leave this source-specific claim undecided rather than denying expression or inferring a wrong gene. Supporting Evidence: |
| GO:0030222 eosinophil differentiation | IEP PMID:8507862 Expression of mRNA for the GATA-binding proteins in human eo... | ACCEPT | Summary: GATA1 supports eosinophil differentiation through a lineage transcriptional program. Reason: PMID:8507862 provides genuine expression-pattern evidence in human eosinophils and induced HL-60 sublines; that original IEP context is not upgraded to a perturbation code. Independent original PMID:12045236 experiments with human CD34-positive cells and mouse deficiency/rescue directly support GATA1-dependent eosinophil development. The human recipient and the source’s mouse cDNA constructs remain distinguished. |
| GO:0048821 erythrocyte development | IMP PMID:10700180 Familial dyserythropoietic anaemia and thrombocytopenia due ... | ACCEPT | Summary: GATA1 supports progression of erythrocytes toward mature identity. Reason: The original V205M study establishes a cofactor-dependent erythroid defect in the human disease and experimental differentiation contexts. Independent original studies of GATA1-dependent erythroid maturation corroborate the role. This cellular developmental process is distinguished from the same source’s uncertain gonadal phenotype and from an inferred whole-organ morphogenesis claim. |
| GO:0070527 platelet aggregation | IMP PMID:15701726 Selective impairment of platelet activation to collagen in t... | KEEP AS NON CORE | Summary: The human R216Q and mouse deficiency study shows selective platelet aggregation impairment. Reason: The authentic abstract explicitly reports collagen and shear-associated aggregation defects, preserved responses to G protein-coupled receptor agonists and effects not wholly explained by platelet count or GPVI abundance. This supports the original IMP phenotype as non-core relative to GATA1’s lineage-regulatory functions. The exact underlying GPVI biosynthesis mechanism remains a separate unresolved claim. Supporting Evidence: |
| GO:0070742 C2H2 zinc finger domain binding | IPI PMID:12483298 Molecular cloning and characterization of the GATA1 cofactor... | UNDECIDED | Summary: GATA1–FOG1 binding is established, but the precise C2H2-domain assertion is not yet verified. Reason: The official GO:0070742 definition specifically requires binding to a C2H2 zinc finger. PMID:12483298 directly supports human FOG1 interaction and finger-dependent differences, but the accessible original publisher content is a subscription abstract, not the full domain-mapping assays. Mixed finger classes in FOG1 make it unsafe to infer the exact contacted class from the protein name or general cofactor association. Retain the original IPI record as undecided pending the relevant original assay rather than claiming wrong-gene evidence or a contradicted interaction. Supporting Evidence: |
| GO:0003677 DNA binding | IDA PMID:8628290 A palindromic regulatory site within vertebrate GATA-1 promo... | MODIFY | Summary: GATA1 recognizes a palindromic element within GATA1 promoters. Reason: The authentic PMID:8628290 abstract describes the GATApal regulatory sequence, finger dependence and promoter effects after partial-motif deletion. The retained PMC HTML provides the abstract and links to scanned pages, not an inspected full Methods section, so exact construct species is not inferred. This positive source scope and independent human promoter evidence support refinement to GO:0000978 without denying the original DNA-binding experiment. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
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Download this section (compressed HTML)Q: Which target-occupancy and cofactor-recruitment mechanisms distinguish the 335-residue splice product from full-length GATA1 and 330-residue GATA1s in matched human cells, beyond the established N-terminal transactivation and short-form-only erythropoietic differences?
Q: Which original assays support the unresolved source-specific glycoprotein-biosynthesis, Sertoli-development and absent-ligand apoptotic-process contexts? Accessible abstracts or distinct rescue conditions do not resolve those precise claims.
Q: Can the exact FBF1/Q8TES7-6 sequence be joined to the tested HI-II-14 clone for the GATA1–FBF1 pair? Accession-to-gene identity and the positive gene-level pair are established; only that pair-specific clone equivalence remains unresolved.
Q: Does direct mapping of the original FOG1 interaction surface support the incoming C2H2-zinc-finger-domain term, given the need to distinguish GATA1 and FOG1 domain orientations?
Experiment: Compare sequence-verified human P15976-1, P15976-2 and P15976-3 at matched expression in the same hematopoietic progenitor background, measuring chromatin occupancy, FOG1/Mediator recruitment and erythroid, megakaryocytic and eosinophil outputs separately.
Experiment: Resolve source-specific platelet glycoprotein effects by separating transcription, new protein synthesis, surface trafficking and turnover in matched wild-type and variant human megakaryocytic cells.
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