GATA3 recognizes GATA motifs and regulates RNA-polymerase-II transcription through context-dependent coactivators and corepressors. Direct binding to nucleosomal DNA is a second, experimentally separable mechanism. The review therefore uses two molecular-function cores, while retaining immune, epithelial and organ-development contexts in their individual annotation assessments.
The current review contains 197 original annotation contexts and one refined inherited NEW proposal. The parser produces 196 keys because two original activator assertions share its key; the two originals differ in assertion ID, assigning database and date and remain separately represented. The original snapshot and mapping are in the source-evidence file. It also preserves the original qualifiers, WITH/FROM entities and dates, including four extension atoms omitted by the parser. This is source-metadata restoration, not four new biological assertions.
PMID:2017177(https://pubmed.ncbi.nlm.nih.gov/2017177/) establishes human and murine GATA-factor DNA recognition and transcriptional activation. The active core contains one short exact anchor; the original source's human and mouse scopes are distinguished from individual modern human product identities.
PMID:17075044(https://pubmed.ncbi.nlm.nih.gov/17075044/) supports FUT7 repression and interactions with T-bet and HDAC proteins. Selected original Results, Methods and textual figure captions were read. PMID:20484083(https://pubmed.ncbi.nlm.nih.gov/20484083/) was recovered beyond its partial cache: Menin–GATA3 cell-free binding is positive, c-Myb binary interaction is weak and strengthened by Menin, and direct GATA3–MLL IP binding was not found. ReChIP co-occupancy is not substituted for direct binding. The coactivator, corepressor and transcription-factor binding refinements retain these distinctions.
PMID:19805038(https://pubmed.ncbi.nlm.nih.gov/19805038/) supports shared genomic targets and opposing T-cell programs. The selected original Methods, Results, Discussion and textual captions were read, including failed sequential-ChIP controls. It does not establish symmetric physical inhibition of T-bet and GATA3 or a direct motility assay. PMID:19674970(https://pubmed.ncbi.nlm.nih.gov/19674970/) supplies human endothelial Tie2 promoter, occupancy, mutagenesis and Ang1-response evidence. ELF1 binding is reported; ELF2 transcriptional synergy alone does not resolve its separate physical-binding annotation.
Five positive generic protein-binding screen annotations are removed for lack of functional information, without denying their measured interactions. More informative binding terms are used only where the inspected source supports them. The unresolved ELF2 interaction remains UNDECIDED. The target-pair checks include actual supplementary tables from PMID:25416956, PMID:25910212, PMID:26871637 and PMID:32814053; selected target cells and original retrieval links for the questioned sources are now in the external-evidence page; yeast constructs and screen-specific isoform distinctions remain explicit. A screen's title or foreground gene was not used as a reason to reject the target.
Official direct sequences establish P23771-1 as 443 residues and P23771-2 as 444 residues. VSP_001598 replaces T259 with TE. No distinct physiological function is assigned to either natural product solely from a construct experiment.
The original PMID:28473536(https://pubmed.ncbi.nlm.nih.gov/28473536/) SELEX supplement contains GATA3 in Supplementary Table S1, row 295. Its full-length 444-residue sequence matches product 2; the 144-residue extended DNA-binding construct matches product 1 residues 238–381. S2 rows 8198/8203 and 8208/8213 distinguish methylated and unmethylated full-length experiments. The table supports sequence-specific binding; promoter specificity and transcriptional function use independent evidence. No binding affinity or product-exclusive phenotype is inferred from the matrix.
PMID:32811816(https://pubmed.ncbi.nlm.nih.gov/32811816/), the original article, uses an explicitly human P23771-2-derived fragment, residues 261–371. Purified nucleosome binding, motif controls and a cryo-EM complex support GO:0031491 nucleosome binding. It is an actual is_a descendant of the inherited proposed GO:0003682 chromatin binding, so the proposal is refined rather than duplicated. Selected Methods, Results and textual captions were read; images and full supplements were not independently inspected. Nucleosome engagement is distinguished from productive opening and from ATP-dependent remodeling chemistry.
PMID:38281186(https://pubmed.ncbi.nlm.nih.gov/38281186/) uses inducible GATA3 and CHD4 perturbation in human MDA-MB-231 cells. CHD4 constrains inappropriate accessibility at GATA3-bound sites; the remodeling activity is not assigned to GATA3. PMID:38923989(https://pubmed.ncbi.nlm.nih.gov/38923989/) concerns a distal enhancer regulating the GATA3 locus, with human correlations and context-dependent mouse deletion results. Locus contacts do not establish GATA3 protein as the loop-forming effector. These selected original scopes, not entire-paper or image inspection, support the synthesis.
Human target evidence and traced mouse or rat donor experiments are kept separate. A broad signal-transduction term can include a transcriptional relay. This does not automatically establish participation in each specific upstream pathway. The inspected PMID:20696860 experiments regulate GATA3 translation downstream of TCR–PI3K/mTOR; they do not test GATA3 as the executor of those signaling steps. In PMID:19112489, Gata3 links beta-catenin activity to Ret, while canonical Wnt response genes remain responsive after Gata3 loss. Those distinct scopes govern the specific signaling assessments.
The original nephric-duct study supports kidney and duct phenotypes without equating collecting-duct identity with nephron-tubule epithelial differentiation. Male reproductive-duct defects are distinguished from male-gonad development. Uterine agenesis remains a positive observation, while the study proposes an indirect obstruction mechanism from neighboring ectopic buds. Lens BrdU/Ki67 results in PMID:19623612 support a context-specific cell-cycle phenotype; direct p27/p57 regulation and causal ordering remain unresolved. In PMID:34644537, macrophage Gata3 deletion impairs IL-33-associated polarization and resolution while leaving the tested IL-4 response intact.
Cochlea and duct evidence is centralized in the external-evidence page.
All nine IBA contexts were traced through the actual PTHR10071 family tree, alignment, node lookup and literal IBD records. The human target is AN265/PTN002467677, with an exact 443-residue match. The 472-node tree, 255 leaves and 2,602-column alignment place it below each asserted ancestor without a retained target-path loss. Target self-donors are legitimate experimental grounding, and donor count is not a weakness test. One dated donor-set difference is retained separately from the incoming original assertion.
Reproducible upstream inputs are the PANTHER 19 tree, alignment, sequences, attributes, node lookup and IBD file. Their inspected byte hashes and literal placements are in the evidence file. The canonical PAINT TSV alone is not claimed to prove a tree or sequence relationship.
Sixteen current Reactome location references were inspected as actual curated event/entity chains. Human P23771 is explicitly present at nucleoplasm through typed component/member relationships, including alternative sets. This verifies model participation and location, without claiming that every member of an alternative set coexists or that GATA3 performs another component's chemistry. The event-cited primary papers were not all read independently. HPA's supported-nucleoplasm XML was inspected; the underlying images were not.
The prior review, five history records, provider reports, analysis scripts and outputs remain unchanged at the inherited Git snapshot. Exact object locators are in the evidence file. There are 257 inherited original annotations plus one prior NEW, with 77 originals absent from the current snapshot. Their retirement is a source change, not a biological refutation.
All 181 historical quote associations remain recoverable from the exact inherited review. The audit found 71 literal matches, 87 whitespace-only matches and 23 without a literal match. Literal matching alone does not prove claim support. The old pioneer quote attributed to PMID:23818516 is invalid: that PMID identifies a transplantation review. It is retained historically and excluded from active support. The two prior DISPUTED sidecar findings and LOW_QUALITY source assessment remain explicit: an expanded STRING network is not a set of validated direct interactions, and a hardcoded target list is not independent validation.
The five original exact excerpts remain unchanged. Short cached abstract excerpts now anchor the ECM1 receptor-binding distinction and the independent cochlear-wiring evidence, and two original core anchors are repeated once in the appended biological notes. The ledger counts all repeated occurrences across review and notes: PMID:2017177 has 16 words, PMID:32811816 has 18, PMID:21217760 has 12, PMID:23426694 has 8, and the other original sources have 4, 9 and 8. Every source remains within the 25-word aggregate limit. Hashes and offsets record the evidence without repeating the quote text in the ledger. External table cells are selected factual identifiers and assay values, not claims that abstract-only caches contain those tables.
There are 92 manual reference assessments: 62 papers, 16 Reactome entries, ten GO method references, three inherited local sources and UniProt. The wider normal-source union contains 71 papers, 24 Reactome records and three PANTHER files; additional bibliography/pathway caches are not represented as fully read merely because they are in that union. Genuine native refresh reconciled all 197 exporter rows and 196 parser keys, retaining both colliding originals and restoring the four literal extension atoms. All current excerpts match unchanged cache bytes; four machine titles differ only in typography. The source union has 97 present caches: 65 exact reused objects and 32 missing-only acquisitions. R-HSA-983231 remains absent and reserved to the GATA2 owner after its retained service failures; it was not fetched or synthesized here. Source availability is distinct from the selected reading recorded in each assessment. Default validation, strict GOA matching, native EDIT history validation and private rendering pass. The computed status is DRAFT; one advisory notes the uncited historical deep-research artifacts. The ontology cache and all 97 present sources remain unchanged.
The newly acquired originals for PMID:12923059 and PMID:20636338 permitted selected Methods/Results reading of the skin-graft/null-allele experiment and the GATA3/MTA2 association, occupancy and reporter experiments. Earlier access failures remain historical; images, complete papers and purified binary GATA3/MTA2 binding are not claimed. These access updates do not change the approved decisions.