FOXP1 is a forkhead DNA-binding transcription factor that regulates gene expression in the nucleus through sequence-specific DNA recognition and association with transcriptional partners. It can recruit the SMRT corepressor and repress targets involved in myeloid differentiation, lymphocyte survival and other developmental programs. Its transcriptional effect depends on the target and cellular context: FOXP1 activates selected targets such as FBXL7, and an embryonic-stem-cell splice form changes DNA-binding preference and regulates pluripotency-associated genes. Human pathogenic variants link FOXP1 to neurodevelopment, while human vascular-cell and lymphocyte experiments and mammalian models establish additional context-dependent roles in cell migration, differentiation, growth and survival. Alternative splicing changes the DNA-binding and other regions of the protein.
Definition: Any process that stops, prevents, or reduces the frequency, rate or extent of the differentiation of a relatively unspecialized T cell into a mature T follicular helper cell.
Justification: The original mouse Foxp1 study PMID24859450 specifically measures restraint of follicular-helper differentiation. GO:0045623 preserves the demonstrated regulatory direction but is broader in cell subtype; GO:0061470 denotes differentiation itself. No dedicated negative-regulation child of GO:0061470 was found in the checked ontology. This is an ontology-development proposal, not an additional annotation or a claim that mouse Foxp1A/D constructs identify human natural isoforms.
Parent term: negative regulation of T-helper cell differentiation
Supporting Evidence:
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000122 negative regulation of transcription by RNA polymerase II | IEA GO_REF:0000108 | ACCEPT | Summary: Negative regulation of Pol II transcription is a core biological output. Reason: The original ontology-based inference from GO:0001227 is corroborated by human FOXP1 repression of c-fms and SV40 reporters and regulation of endogenous proapoptotic target genes. Repression is target- and context-dependent; selected activation elsewhere does not invalidate these positive negative-regulation experiments. |
| GO:0000785 chromatin | ISA GO_REF:0000113 | ACCEPT | Summary: FOXP1 acts at chromatin-associated regulatory regions. Reason: The TFClass chromatin annotation is independently supported by regional promoter ChIP and human B-cell ChIP-seq combined with expression perturbations. Chromatin occupancy does not alone define a precise DNA-contact interface, and the bacterial specificity fragment provides complementary evidence. Retain the cellular location as part of the transcriptional mechanism. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: FOXP1 recognizes cis-regulatory DNA sequences. Reason: The actual human AN14/PTN002483645 leaf descends from the asserted Bilateria node PTN000215041, and the literal IBD donors match this original row. Human full-length MFH/FOXP1 repressed c-fms reporters, with a human 431–559 GST fragment and mutant oligonucleotides establishing sequence-dependent promoter binding in PMID15286807. The human FOXP1 fragment in PMID28473536 independently yielded specific DNA motifs. Retain the phylogenetic annotation; donor number is not a confidence score, and the off-target family alignment discrepancy does not involve the exact human sequence. |
| GO:0000981 DNA-binding transcription factor activity, RNA polymerase II-specific | ISA GO_REF:0000113 | TOO GENERAL | Summary: The Pol II transcription-factor class is correct but broader than the established repressor activity. Reason: The TFClass assignment agrees with human promoter-binding and reporter experiments. GO:0001227 is an is_a subtype of this term and captures the established DNA-binding repressor activity more precisely. FOXP1 can also enhance selected targets in particular cellular or splice-form contexts; this broadness decision does not assert that it invariably represses every target. |
| GO:0001046 core promoter sequence-specific DNA binding | IDA PMID:28218735 Aurora kinase A regulates Survivin stability through targeti... | MODIFY | Summary: Use supported Pol II cis-regulatory DNA binding without an unresolved core-promoter boundary claim. Reason: Selected original PMID28218735 establishes regional FBXL7 promoter occupancy and reporter responses to FOXP1, including deletion constructs, but those experiments do not independently delimit a sequence-specific interaction with the basal core promoter. The broader cis-regulatory binding function is directly supported by the human c-fms oligonucleotide/EMSA and reporter experiments in PMID15286807. Replace the overly narrow term with GO:0000978 while retaining this exact original source row; the independent support is not represented as a core-promoter assay in PMID28218735. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding |
| GO:0001227 DNA-binding transcription repressor activity, RNA polymerase II-specific | IBA GO_REF:0000033 | ACCEPT | Summary: DNA-binding transcriptional repression is a principal FOXP1 activity. Reason: The original Deuterostomia IBD at PTN000215042 lies on the verified human target path, with literal descendant evidence preserved. Human MFH/FOXP1 sequence-dependent c-fms repression and full-length FOXP1 SV40 reporter repression independently support the function. Artificial disease variants, bacterial DNA-binding fragments and the seven natural products are distinguished; the annotation does not establish equivalent activity of every product. |
| GO:0002903 negative regulation of B cell apoptotic process | IDA PMID:25267198 FOXP1 directly represses transcription of proapoptotic genes... | KEEP AS NON CORE | Summary: FOXP1 limits apoptosis in an activated human B-cell context. Reason: Original PMID25267198 human primary memory-B-cell experiments show reduced caspase-dependent apoptosis and increased survival with CD40L or constitutive IKK2 signaling. Dye dilution did not show extra proliferation, and repression persisted without the survival benefit when the cooperating signal was absent. Retain the specific antiapoptotic process as non-core; it is a context-dependent consequence of transcriptional regulation, not universal B-cell survival activity. Supporting Evidence: |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000002 | TOO GENERAL | Summary: Generic DNA-binding transcription-factor activity is less precise than the Pol II repressor function. Reason: The InterPro domain assignment is biologically consistent with the directly established human transcription factor. The accepted GO:0001227 lies below GO:0003700 through an is_a path. Preserve the original electronic sources and use the more informative existing function. |
| GO:0005515 protein binding | IPI PMID:18347093 Cooperative regulation in development by SMRT and FOXP1. | MODIFY | Summary: FOXP1 binds and recruits the SMRT transcription corepressor. Reason: The original selected Methods explicitly combine human FOXP1 with mouse SMRT, matching the retained Q9WU42 partner. Coimmunoprecipitation/GST interaction experiments and human THP1 knockdown/ChIP support functional corepressor recruitment to c-fms. Official Q9WU42 metadata identifies nuclear receptor corepressor 2 and experimental corepressor activity. GO:0001222 expresses the supported binding class; this does not make FOXP1 itself a corepressor lacking DNA-binding activity or establish a fixed native complex stoichiometry. Proposed replacements: transcription corepressor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:18640093 FOXP1 is an androgen-responsive transcription factor that ne... | MODIFY | Summary: The original partner is the androgen nuclear receptor. Reason: The authentic PMID18640093 abstract explicitly reports FOXP1–AR interaction and ligand-dependent repression in prostate cancer cells; exact full Methods remain uninspected. Official P10275 metadata independently establishes androgen nuclear receptor activity. Refine the binding class to GO:0016922, preserving P10275 and the original source. This class-level judgment does not invent a purified assay or assign the historical FOXP1D construct to a current natural isoform. Proposed replacements: nuclear receptor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:19907493 Human-specific transcriptional regulation of CNS development... | MODIFY | Summary: FOXP1 associates with the Pol II transcription factor FOXP2 in the nucleus. Reason: Original PMID19907493 Methods and Results actually examine FOXP1 by nuclear colocalization and coimmunoprecipitation/immunoblot or mass spectrometry with FOXP2 constructs in SH-SY5Y cells. The FOXP2-focused title is not a wrong-gene indication. Official O15409 Pol II transcription-factor classification supports GO:0061629. Keep the original occurs_in nucleus extension; cellular association does not establish isolated binary affinity or native oligomer stoichiometry. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:24893771 Investigating protein-protein interactions in live cells usi... | MODIFY | Summary: Live-cell proximity supports FOXP1 association with FOXP2. Reason: Selected original PMID24893771 Results/captions and two exact retained IntAct records recover FOXP1–FOXP2 BRET in both donor/acceptor directions with nuclear-localized controls. O15409 is an officially classified Pol II DNA-binding transcription factor, supporting GO:0061629. Preserve the nuclear extension. BRET establishes proximity in the tested tagged-cell context; the full original protocol and unique natural product identity were not independently resolved here. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | MODIFY | Summary: Human FOXP1 coimmunoprecipitates with FOXP2. Reason: The recovered author-hosted PMID25027557 original identifies sequenced human BC152752, a 677-aa FOXP1 ORF, and tagged FOXP1/FOXP2 coimmunoprecipitation in HEK293 cells. Official O15409 classification supports the specific Pol II transcription-factor-binding term. Combination-dependent expression does not isolate pure heterodimer action. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | MODIFY | Summary: The nuclear FOXP1–FOXP2 interaction has a specific transcription-factor partner class. Reason: PMID25027557 selected original coimmunoprecipitation and nuclear microscopy support association of human FOXP1 with FOXP2 in the tested HEK293 setting. Official O15409 Pol II transcription-factor metadata justifies GO:0061629. The original nuclear scope is retained. No unique native oligomer composition is inferred. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | MODIFY | Summary: Human FOXP1 associates with the Pol II transcription factor FOXP4. Reason: The recovered PMID25027557 Methods/Results directly test tagged human FOXP1 with FOXP4. Official Q8IVH2 identifies FOXP4 and Pol II DNA-binding transcription-factor activity, allowing GO:0061629. Gene-expression changes in cotransfected cells do not prove exclusive heterodimer causation. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | MODIFY | Summary: The nucleus-restricted FOXP1–FOXP4 association can be refined by partner class. Reason: Original PMID25027557 coimmunoprecipitation and microscopy support the tested nuclear association. Q8IVH2 is an officially classified Pol II DNA-binding transcription factor. Use GO:0061629 with the original nuclear scope. The 677-aa human construct is established; no untested natural-product functional equivalence is inferred. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25609649 Proteomic analyses reveal distinct chromatin-associated and ... | MODIFY | Summary: FOXP2 association is verified in the original chromatin and soluble proteomic fractions. Reason: Original PMID25609649 Table S6 (HCIP) recovers FOXP2 with FOXP1 bait in the chromatin fraction (row 1825; 10 spectra, SAINT 1) and soluble fraction (row 1839; 7 spectra, SAINT 1), with reciprocal soluble recovery of FOXP1 by FOXP2 (row 1859). The chromatin fraction supports the retained nuclear context; the soluble fraction alone does not distinguish nuclear from cytosolic pools. Official O15409 Pol II transcription-factor class supports GO:0061629. Independent human association assays in PMID19907493, PMID25027557 and PMID26647308 corroborate the partner pair. Preserve the original citation, partner and nuclear extension; these cellular complex recoveries do not establish isolated binary affinity or map the experimental clone to a current natural isoform. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005515 protein binding | IPI PMID:25609649 Proteomic analyses reveal distinct chromatin-associated and ... | MODIFY | Summary: Original fraction-specific FOXP4 association supports the specific transcription-factor binding class. Reason: Original PMID25609649 Table S6 (HCIP) recovers FOXP4 with FOXP1 bait in chromatin (row 1826; 10 spectra, SAINT 1) and soluble material (row 1835; 17 spectra, SAINT 1); FOXP4 bait reciprocally recovers FOXP1 in chromatin and soluble fractions (rows 1913 and 1919). Chromatin recovery supports the original nuclear extension, while the soluble pool is not nuclear-specific. Independent PMID25027557 human coimmunoprecipitation and nuclear localization corroborate the pair. Official Q8IVH2 Pol II transcription-factor class supports GO:0061629. Preserve the original source and partner; TAP/MS complex recovery does not establish isolated binary affinity or a current natural-product assignment. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005515 protein binding | IPI PMID:25853299 A de novo FOXP1 variant in a patient with autism, intellectu... | MODIFY | Summary: FOXP1 interaction with FOXP2 can be refined while preserving variant and localization limits. Reason: Recovered PMID25853299 selected Methods/Results include tagged WT and V423Hfs*37 constructs, BRET interaction with FOXP2 and altered localization on mutant coexpression. The original annotation is not explicitly mutant-restricted; independent WT nuclear FOXP1–FOXP2 evidence is also available in PMID25027557 and PMID26647308. Refine to GO:0061629 and preserve the original nuclear scope. Patient lymphoblast RNA showed nonsense-mediated decay, so transfected mutant effects do not prove appreciable mutant protein accumulates in the patient. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005515 protein binding | IPI PMID:26647308 Identification and functional characterization of de novo FO... | MODIFY | Summary: The FOXP2 association has a verified Pol II transcription-factor class. Reason: Original PMID26647308 selected functional Results and BRET Methods directly test FOXP1/FOXP2 proximity with nuclear controls; exact current IntAct records corroborate that pair. O15409 classification supports GO:0061629. Patient variants are artificial experimental constructs and do not identify natural alternative products or establish a universal dominant-negative mechanism. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:26647308 Identification and functional characterization of de novo FO... | MODIFY | Summary: Retain and refine the distinct nuclear FOXP1–FOXP2 binding context. Reason: PMID26647308 selected BRET/localization assays and independent WT nuclear interaction evidence support the same partner class. Use GO:0061629 with the original occurs_in nucleus atom intact. Some transfected disease variants mislocalize partners; those conditions are not generalized to all WT nuclear interactions or natural products. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005515 protein binding | IPI PMID:28218735 Aurora kinase A regulates Survivin stability through targeti... | MODIFY | Summary: FOXP1 associates with the protein kinase AURKA. Reason: Selected original PMID28218735 Figure 7b shows reciprocal recovery of transfected His-FOXP1 and AURKA from HEK293T lysates, complementing GST-AURKA capture from AGS cell extracts. Official O14965 metadata establishes experimentally supported protein kinase activity, so GO:0019901 specifies the partner class. This is cellular association in the FOXP1–FBXL7 regulatory context; it does not assign kinase activity to FOXP1 or establish isolated binary affinity, a native interface, or a kinase-adaptor mechanism. Proposed replacements: protein kinase binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:30250039 Functional characterization of TBR1 variants in neurodevelop... | MODIFY | Summary: FOXP1 associates with the Pol II transcription factor TBR1. Reason: Original PMID30250039 live-cell HEK293 BRET uses sequenced FOXP1 NM_032682 and TBR1 WT/variant fusion constructs with nuclear controls. Official Q16650 metadata establishes TBR1 Pol II transcription-factor activity. GO:0061629 is a supported class refinement. The tested association does not establish transcriptional cooperation, isolated affinity or an endogenous complex stoichiometry. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | MODIFY | Summary: FOXP2 is the specific partner in a positive proteomic association. Reason: Three exact retained PMID33961781 IntAct records identify the original FOXP1–FOXP2 pair in tagged affinity-purification experiments from HEK293T and HCT116 cells, with spoke-expanded association metadata. Independent nuclear coimmunoprecipitation/BRET supports the same partner pair. Refine to GO:0061629 using official O15409 Pol II transcription-factor class, retaining the original nuclear extension. The original supplement and its fraction-level localization were not inspected, and AP-MS does not establish direct contact. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding |
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: Nuclear activity is consistent with the verified phylogeny and direct human experiments. Reason: The original PTN000215041 IBD is on the actual human target path and includes human FOXP1 among its legitimate descendant evidence. Self-donor evidence is not circular. Human nuclear microscopy, chromatin occupancy and reporter assays independently support nuclear transcriptional activity. Preserve is_active_in and all donor groupings; tagged or mutant localization conditions are not generalized to every natural product. |
| GO:0005634 nucleus | IDA PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | ACCEPT | Summary: The original human construct localizes to the nucleus. Reason: Recovered PMID25027557 uses sequenced human 677-aa BC152752 FOXP1 and nuclear microscopy in HEK293 cells. Retain the nuclear localization annotation. Supporting Evidence: |
| GO:0005634 nucleus | IDA PMID:26647308 Identification and functional characterization of de novo FO... | ACCEPT | Summary: WT human FOXP1 nuclear localization is directly supported. Reason: Recovered PMID26647308 localization experiments establish nuclear WT FOXP1, with distinct effects of artificial patient variants. Retain the original unrestricted nucleus row while keeping those variant-dependent outcomes explicit. The experiments do not identify localization of all seven natural products. Supporting Evidence: |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: Nuclear localization is well supported. Reason: The UniProt subcellular-location mapping agrees with original human WT FOXP1 microscopy and endogenous/chromatin-associated activity. This does not imply that the short 114-aa natural product or every disease construct has been experimentally localized. |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: Official HPA immunofluorescence supports nucleoplasmic localization. Reason: The authentic HPA XML for ENSG00000114861 identifies ICC/IF with supported reliability and a main GO:0005654 nucleoplasm location, with named human cell-line image metadata. Assay metadata were inspected; image pixels and antibody validation experiments were not independently reanalyzed. Human nuclear/chromatin experiments provide independent biological corroboration. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-1112609 | ACCEPT | Summary: Nucleoplasmic activity is consistent with the Reactome transcriptional event. Reason: The immutable original Reactome R-HSA-1112609 record names FOXP1-ES in a POU5F1-promoter event. Independent human FOXP1 nuclear experiments and the selected PMID21924763 stem-cell context support nucleoplasmic function. Preserve the original unrestricted GOA product; the event does not establish that all seven products share the FOXP1-ES DNA preference or activity. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-480204 | ACCEPT | Summary: Nucleoplasmic localization is independently established despite the abbreviated event summary. Reason: The original cached R-HSA-480204 summary describes NANOG promoter regulation without a detailed FOXP1 participant record. That summary alone is not a full event audit or evidence of wrong citation. Independent human nuclear microscopy and FOXP1-ES transcriptional studies support the same nucleoplasmic location. Keep the original source and avoid assigning an isoform-specific event to every natural product. |
| GO:0005667 transcription regulator complex | IEA GO_REF:0000117 | ACCEPT | Summary: FOXP1 participates in transcription-regulatory protein assemblies. Reason: The ARBA complex annotation agrees with functional SMRT recruitment and human FOXP-family coimmunoprecipitation linked to transcriptional regulation. Retain this generic transcription-regulator-complex membership. The evidence does not define one constitutive native assembly or a universal subunit stoichiometry. |
| GO:0005667 transcription regulator complex | IPI PMID:20950788 De novo mutations in FOXP1 in cases with intellectual disabi... | ACCEPT | Summary: Complex participation is independently supported, with this original paper’s assay scope retained. Reason: Selected PMID20950788 establishes human FOXP1 reporter repression; its CTBP1-interacting region is a prior-work annotation, not a new complex assay in that paper. Independent human FOXP1/SMRT and FOXP1/FOXP2/4 functional association experiments support the unrestricted transcription-regulator-complex term. Retain the original IPI/source object without falsely claiming an independently verified complex assay in PMID20950788. |
| GO:0005667 transcription regulator complex | IPI PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | ACCEPT | Summary: Human FOXP1 is recovered in functional transcription-factor assemblies. Reason: Original PMID25027557 human 677-aa FOXP1 coimmunoprecipitates with FOXP2/FOXP4 and alters target-gene expression in combination-dependent cell assays. This supports transcription-regulator-complex participation, while neither a pure heterodimer mechanism nor unique native stoichiometry is established. Preserve the original IPI source. Supporting Evidence: |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000002 | TOO GENERAL | Summary: General DNA-templated transcription regulation is broader than the supported Pol II functions. Reason: The InterPro-based annotation is consistent with FOXP1 biology, but the accepted Pol II repressor activity and negative regulation of Pol II transcription give greater functional specificity. The original electronic fields remain intact. |
| GO:0006357 regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | TOO GENERAL | Summary: The PAINT transcription-regulation assertion is valid but broad. Reason: The human leaf lies below the literal PTN000215041 IBD, with original donors preserved. The current exact-term queries do not recover every historical donor BP row, which is a query/time limitation and does not refute the authentic ancestral assertion. More specific Pol II repression is directly supported in human experiments. The general term is therefore less informative; target-specific activation in other contexts remains described separately. |
| GO:0006974 DNA damage response | IMP PMID:30111844 MicroRNA miR-34a downregulates FOXP1 during DNA damage respo... | KEEP AS NON CORE | Summary: FOXP1 participates in a contextual B-cell signaling response to DNA damage. Reason: Recovered original PMID30111844 shows FOXP1 downregulation through the DDR–p53–miR-34a axis and a functional effect of FOXP1 siRNA on BCR calcium flux and AKT/ERK responses in human cells. Retain the existing broad DNA-damage-response association as non-core. These experiments concern a transcriptional/signaling response to damage, not DNA repair catalysis or direct lesion sensing by FOXP1. Supporting Evidence: |
| GO:0010468 regulation of gene expression | IMP PMID:28218735 Aurora kinase A regulates Survivin stability through targeti... | MODIFY | Summary: FOXP1 positively regulates FBXL7 transcription in the tested cellular context. Reason: Selected original PMID28218735 Figure 7e–f and the corresponding Results show increased FBXL7 promoter-reporter activity after FOXP1 expression in HEK293T cells, including responses of promoter deletion constructs; AURKA suppresses this FOXP1-dependent activation. GO:0045944 captures the supported positive transcriptional direction more precisely than regulation of gene expression. Regional promoter occupancy complements the reporter result but does not establish a particular direct DNA-contact boundary. This target-dependent activation does not imply that FOXP1 universally activates transcription or that every natural product has the same output. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: |
| GO:0010595 positive regulation of endothelial cell migration | IMP PMID:24023716 FoxP1 stimulates angiogenesis by repressing the inhibitory g... | KEEP AS NON CORE | Summary: FOXP1 supports migration of cultured human endothelial cells. Reason: Original PMID24023716 human HUVEC knockdown/overexpression experiments measured planar migration as well as other angiogenic phenotypes. Retain this positive regulation as a non-core cellular context. The source is not a direct assay of an extracellular motility factor, and the transcript/68-kDa wording does not identify a current natural isoform. Supporting Evidence: |
| GO:0010629 negative regulation of gene expression | IDA PMID:30111844 MicroRNA miR-34a downregulates FOXP1 during DNA damage respo... | KEEP AS NON CORE | Summary: FOXP1 negatively regulates CD22 expression in the tested B-cell setting. Reason: Selected original PMID30111844 reports increased CD22 surface abundance after FOXP1 siRNA and inverse FOXP1/CD22 expression in CLL samples. The earlier promoter-binding result is cited prior work, not a new binding assay in this paper. Preserve the original has_input UniProtKB:P20273 atom and non-core expression-regulation context. This extension does not establish a physical interaction between FOXP1 protein and the CD22 receptor. Supporting Evidence: |
| GO:0021756 striatum development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: FOXP1 has a supported non-core role in striatal development. Reason: Independent PMID25266127 mouse Nestin-Cre Foxp1 deletion reduces the tyrosine-hydroxylase-defined striatal region from early postnatal stages and alters striatal transcription and neuronal morphology. This functional developmental evidence supports retaining the existing regional process beyond the original rat expression transfer. The human IEA still retains Q498D1 and its Ensembl donor: the traced rat PMID12815709 IEP source remains abstract-only and is not relabeled as a knockout assay. Broad neural-lineage deletion does not establish a striatum-autonomous mechanism or directly test endogenous human developmental necessity. |
| GO:0030316 osteoclast differentiation | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: Human FOXP1 affects osteoclast differentiation in a transgenic mouse model. Reason: PMID18799727 expresses human FLAG-FOXP1 in mouse monocyte/macrophage lineage cells and reports attenuated osteoclastogenesis/bone resorption. The mouse host does not make this a mouse-protein-only assay. Retain the existing differentiation context as non-core, explicitly noting that maintained FOXP1 expression restrains maturation rather than promoting it. The phenotype does not establish a direct role in bone-resorption chemistry. Supporting Evidence: |
| GO:0030900 forebrain development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: FOXP1 contributes to forebrain development in regional experimental models. Reason: Independent PMID29138280 Emx1-Cre Foxp1 deletion alters developing mouse neocortical size, lamination and neuronal positioning; experimental WT FOXP1 restores the measured migration phenotype, whereas K636R does not. These findings support the existing forebrain-development context as non-core. Human neurosphere K636R-overexpression effects are complementary and are not endogenous human knockout evidence. Preserve the human IEA and original rat Q498D1/Ensembl donors: PMID18561326 remains a source-limited IEP expression study. Regional and possible non-cell-autonomous effects are not generalized into a single direct developmental target mechanism. |
| GO:0032496 response to lipopolysaccharide | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: FOXP1 modulates macrophage responses to LPS in the tested model. Reason: Recovered original PMID18799727 assays LPS-stimulated macrophages carrying a human FOXP1 transgene. In-vitro and in-vivo cytokine panels have different endpoints and statistical outcomes, so they are not conflated. Retain the broad response context as non-core; it does not identify FOXP1 as an LPS receptor or direct cytokine-promoter binder. Supporting Evidence: |
| GO:0032651 regulation of interleukin-1 beta production | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: FOXP1 regulates IL-1 beta production in a defined macrophage assay. Reason: In PMID18799727, transgenic human FOXP1 reduced IL-1 beta in cultured LPS-stimulated mouse macrophages, and an independent functional c-Fms rescue restored the cytokine defect. The in-vivo six-hour IL-1 beta comparison was not significant and is not used as confirming evidence. Retain the source-supported regulatory context as non-core without inferring direct IL1B promoter binding. Supporting Evidence: |
| GO:0032655 regulation of interleukin-12 production | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: Retain contextual regulation of IL-12 production. Reason: Original PMID18799727 Table3 reports reduced IL-12 after overnight LPS stimulation of human-FOXP1-transgenic mouse macrophages. This supports a non-core regulatory effect in that model. The source does not establish a general cytokine-producing activity of FOXP1 or a direct IL12-promoter mechanism. Supporting Evidence: |
| GO:0032680 regulation of tumor necrosis factor production | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: TNF regulation is supported by the distinct rescue assay, with the initial panel limitation retained. Reason: PMID18799727 Table3 TNF-alpha comparison has p=.057 and is not treated as a significant confirmation. The separate Figure 6D experiment reports restoration of the TNF-alpha defect by c-Fms/M-CSFR overexpression; GFP and K614A controls were included. Keep the annotation as a bounded non-core regulatory context based on that distinct experiment; do not pool the two assay results or claim direct TNF promoter binding. Supporting Evidence: |
| GO:0032745 positive regulation of interleukin-21 production | ISS GO_REF:0000024 | MODIFY | Summary: The exact mouse donor evidence supports negative regulation of IL-21 production. Reason: The human ISS points to mouse P58462; its current same-term IDA PMID24859450 is unnegated involved_in with no extension. Selected original conditional-knockout/transfer and Th1 experiments show increased IL-21 protein/mRNA after Foxp1 loss and suppression by Foxp1D, the opposite of GO:0032745. Propose GO:0032705 while preserving human ISS, original positive term and donor identity. Regional mouse Il21 ChIP supports regulation, not a human assay or a current human product assignment from mouse A/D names. The source-side direction also requires curator review. Proposed replacements: negative regulation of interleukin-21 production Supporting Evidence: |
| GO:0033574 response to testosterone | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: FOXP1 expression responds to androgen in documented cellular contexts. Reason: The rat transfer includes IEP PMID25247470, whose authentic abstract reports androgen-dependent Foxp1 expression; its coimmunoprecipitation result concerns Foxp2 and must not be transferred to Foxp1. Independent human PMID18640093 reports androgen induction of FOXP1 in LNCaP cells and ligand-dependent AR regulation. Retain this non-core response while preserving original rat donor alternatives and keeping response distinct from androgen receptor activity. |
| GO:0036035 osteoclast development | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: Retain supported osteoclast development as a non-core developmental context. Reason: PMID18799727 uses a human FOXP1 CD68 transgene in the mouse monocyte/macrophage lineage and reports restricted osteoclastogenesis and impaired bone resorption. These observations support a context-dependent developmental role alongside the existing osteoclast-differentiation annotation. Retain this broader context as non-core, with human transgene identity and mouse host explicit; the experiment does not establish an equivalent effect of every natural product or an endogenous human osteoclast mechanism. Supporting Evidence: |
| GO:0042116 macrophage activation | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: FOXP1 regulates macrophage activation phenotypes in a contextual model. Reason: Original PMID18799727 human-FOXP1 transgenic macrophages show altered cytokine production, phagocytosis and respiratory burst, with selected c-Fms rescue evidence. Retain the activation context as non-core and describe the observed inhibitory direction. These downstream phenotypes do not establish direct biochemical phagocytic or oxidase activity by FOXP1. Supporting Evidence: |
| GO:0042117 monocyte activation | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: Monocyte activation and maturation are influenced by maintained human FOXP1 expression. Reason: PMID18799727 uses a human FOXP1 transgene and reports reduced c-Fms, migration and macrophage accumulation; blood monocyte numbers were normal. Together with human monocyte-cell experiments in PMID15286807, this supports a non-core regulatory context. Do not conflate normal cell counts with unaffected function or call the transgene a mouse protein. |
| GO:0042118 endothelial cell activation | IMP PMID:24023716 FoxP1 stimulates angiogenesis by repressing the inhibitory g... | KEEP AS NON CORE | Summary: Retain a contextual endothelial activation annotation. Reason: Original PMID24023716 human endothelial perturbations alter proliferation, migration and tube formation. These positive cell-state outcomes support the existing broad activation context as non-core, with the more concrete migration/tube/proliferation endpoints stated separately. The measured effects do not demonstrate direct SEMA5B DNA binding or a uniquely identified natural FOXP1 isoform. Supporting Evidence: |
| GO:0042802 identical protein binding | IPI PMID:25609649 Proteomic analyses reveal distinct chromatin-associated and ... | KEEP AS NON CORE | Summary: Independent self-association evidence supports retention; proteomic bait detection is not a homomerization assay. Reason: Original PMID25609649 Table S6 (HCIP) contains FOXP1 self rows in chromatin and soluble material (rows 1824 and 1833), but their score is explicitly Bait. Detection of the bait itself does not independently demonstrate FOXP1 homomerization, so that source-specific assay question remains unresolved. Original PMID26647308 WT self-association BRET and nuclear localization provide positive independent support for the unrestricted FOXP1 assertion. Preserve the original citation and nuclear extension and retain the association as non-core, without inferring native homodimer stoichiometry or a separate catalytic function. Supporting Evidence: |
| GO:0042802 identical protein binding | IPI PMID:25853299 A de novo FOXP1 variant in a patient with autism, intellectu... | KEEP AS NON CORE | Summary: Self-association is a supported regulatory property with variant-specific assay limits. Reason: Recovered PMID25853299 selected BRET/localization Methods and Results support FOXP1 self-association in tagged cellular contexts; independent WT evidence is present in PMID26647308. Keep the original nuclear extension and non-core interaction. The mutant can mislocalize WT after transfection, but patient RNA undergoes NMD; the assay does not establish mutant-protein abundance or native oligomer composition in vivo. |
| GO:0042802 identical protein binding | IPI PMID:26647308 Identification and functional characterization of de novo FO... | KEEP AS NON CORE | Summary: Retain experimentally supported FOXP1 self-association as a non-core property. Reason: Original PMID26647308 and exact IntAct BRET records support FOXP1 self-association, with nuclear controls and variant-dependent effects. Preserve the nuclear annotation scope. Proximity measurements and colocalization do not determine native oligomer stoichiometry, dissociation constants or equivalent activity across the seven natural products. Supporting Evidence: |
| GO:0043565 sequence-specific DNA binding | IEA GO_REF:0000002 | TOO GENERAL | Summary: Sequence-specific DNA binding is correct but broader than the accepted cis-regulatory binding term. Reason: GO:0000978 entails sequence-specific DNA binding through an is_a path and is supported by human promoter binding. Preserve the electronic InterPro annotation; the broader term is redundant at the level of functional specificity. |
| GO:0045655 regulation of monocyte differentiation | IDA PMID:15286807 Integrin engagement regulates monocyte differentiation throu... | KEEP AS NON CORE | Summary: FOXP1 represses a differentiation program in human monocyte-cell assays. Reason: Original PMID15286807 identifies human 677-aa MFH/FOXP1 and shows that its maintained expression reduces PMA-induced c-fms/CD11b expression, adhesion and phagocytosis in HL60 cells. Sequence-specific c-fms repression provides a mechanistic transcriptional connection. Retain regulation of monocyte differentiation as a non-core physiological context; upstream mouse Mac1 experiments are not a human FOXP1 knockout. Supporting Evidence: |
| GO:0045892 negative regulation of DNA-templated transcription | IDA PMID:20950788 De novo mutations in FOXP1 in cases with intellectual disabi... | TOO GENERAL | Summary: The negative transcriptional effect is more precisely represented as Pol II regulation. Reason: Original PMID20950788 full-length human FOXP1a represses an SV40 luciferase reporter in HEK293 cells, whereas R525X loses activity despite comparable protein. This supports negative transcriptional regulation, but GO:0000122 provides the supported Pol II specificity. Supporting Evidence: |
| GO:0045892 negative regulation of DNA-templated transcription | IMP PMID:26647308 Identification and functional characterization of de novo FO... | TOO GENERAL | Summary: Use the established Pol II specificity for the negative transcriptional function. Reason: Recovered original PMID26647308 WT FOXP1 represses an SV40 reporter, with disease variants losing repression. GO:0000122 captures this transcriptional process more precisely than generic DNA-templated transcription. Variant constructs remain distinct from natural isoforms, and loss of reporter activity does not imply a single shared molecular defect. Supporting Evidence: |
| GO:0045892 negative regulation of DNA-templated transcription | NAS PMID:25027557 Transcriptional regulation by FOXP1, FOXP2, and FOXP4 dimeri... | TOO GENERAL | Summary: Broad negative transcriptional regulation is supported but less precise than the Pol II term. Reason: Recovered PMID25027557 human 677-aa FOXP1 expression and combination-dependent target-gene changes are consistent with transcriptional regulation; independent human promoter-repression experiments establish the more specific Pol II function. Preserve the original NAS evidence and source. Not every cotransfection-dependent transcript is assumed to be a directly bound FOXP1 target. |
| GO:0048513 animal organ development | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Retain broad organ-development involvement as a non-core context. Reason: Human FOXP1 neurodevelopmental variants and mouse SMRT/Foxp1 cardiac genetic studies support organ-development involvement. Retain this broad ARBA context as non-core alongside the established transcriptional mechanism. The supporting clinical and model evidence does not resolve every organ-specific cellular program, and it does not settle the separate regional developmental claims whose original assays remain inaccessible. |
| GO:0048661 positive regulation of smooth muscle cell proliferation | IMP PMID:24023716 FoxP1 stimulates angiogenesis by repressing the inhibitory g... | KEEP AS NON CORE | Summary: FOXP1 supports proliferation in the tested human smooth-muscle cells. Reason: Original PMID24023716 human aortic smooth-muscle-cell knockdown reduces BrdU incorporation. Retain this positive proliferation context as non-core. It is distinct from endothelial assays and does not establish a universal proliferative effect in B cells or other tissues. Supporting Evidence: |
| GO:0048731 system development | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Retain system-development involvement without treating it as the molecular core. Reason: Human neurodevelopmental findings and mouse cardiac developmental genetics support this broad developmental context. Keep the original ARBA annotation as non-core, preserving the distinction between human clinical observations, mouse organ phenotypes and direct transcriptional activity. The broad term does not establish every narrower system or regional claim, and no unsupported subclass entailment is invoked. |
| GO:0050681 obsolete nuclear androgen receptor binding | IDA PMID:18640093 FOXP1 is an androgen-responsive transcription factor that ne... | MODIFY | Summary: Replace the obsolete androgen-receptor-specific binding term with nuclear receptor binding. Reason: Official GO:0050681 obsoletion guidance recommends GO:0016922 with androgen receptor target information, rather than a term named for one gene product. The authentic PMID18640093 abstract reports FOXP1–AR interaction and ligand-dependent regulation, and official P10275 establishes the partner class. Preserve this original obsolete identifier and source; propose GO:0016922 in the review only. AR target information belongs in the explanation or a curator-proposed extension, not a rewritten original machine field. Historical FOXP1D is not assigned to a current product. Proposed replacements: nuclear receptor binding Supporting Evidence: |
| GO:0050727 regulation of inflammatory response | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: FOXP1 influences inflammatory responses through a contextual transcriptional program. Reason: Original PMID18799727 human-FOXP1 transgenic mouse experiments show macrophage functional and peritonitis outcomes, supported by selected cytokine and c-Fms rescue assays. Retain regulation of inflammatory response as non-core, with the actual inhibitory model and assay-specific statistics explicit. The data do not establish a universal anti-inflammatory action in every cell type. Supporting Evidence: |
| GO:0050861 positive regulation of B cell receptor signaling pathway | IMP PMID:30111844 MicroRNA miR-34a downregulates FOXP1 during DNA damage respo... | KEEP AS NON CORE | Summary: FOXP1 supports BCR signaling within the studied DNA-damage-response context. Reason: Recovered original PMID30111844 shows reduced anti-IgM calcium flux and AKT/ERK phosphorylation after FOXP1 siRNA, with unchanged surface IgM. FOXP1 is downregulated during DDR, and CD22 changes provide a possible regulatory connection. Preserve the full original part_of GO:0006974 extension and keep this non-core context; it is not an assay of DNA repair chemistry or a newly measured FOXP1–CD22 physical interaction. Supporting Evidence: |
| GO:0060766 negative regulation of androgen receptor signaling pathway | IDA PMID:18640093 FOXP1 is an androgen-responsive transcription factor that ne... | KEEP AS NON CORE | Summary: FOXP1 can negatively regulate androgen receptor signaling. Reason: The authentic PMID18640093 abstract directly reports ligand-dependent AR repression and androgen-dependent recruitment at the PSA enhancer in human prostate cancer cells. Retain the existing non-core signaling context with the original IDA source. Exact full experimental Methods and the mapping of the historical FOXP1D construct remain unresolved; neither a universal repressor role nor a current isoform assignment is inferred. Supporting Evidence: |
| GO:0061052 negative regulation of cell growth involved in cardiac muscle cell development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Retain the donor-supported restraint of cardiomyocyte growth as a contextual function. Reason: The recovered original PMID26333362 main Methods/Results/Fig7 establish neonatal rat cardiomyocyte Foxp1 knockdown and increased cell size, with reversal of miR-206/YAP-associated hypertrophy by restored Foxp1. This supports the existing rat IMP transfer as non-core growth regulation. Hypertrophy is distinguished from proliferation; the specific overexpression sequence and complete developmental trajectory were not resolved. Supporting Evidence: |
| GO:0061470 T follicular helper cell differentiation | ISS GO_REF:0000024 | MODIFY | Summary: The donor paper establishes inhibition of helper T-cell differentiation. Reason: The exact mouse P58462 IDA PMID24859450 source uses conditional deletion, adoptive transfer and Foxp1A/D expression to show that Foxp1 restrains T follicular helper differentiation. GO:0061470 names differentiation itself; GO:0045623 captures the demonstrated negative regulatory role, with the T follicular helper context retained in the reason. The checked negative-helper-differentiation branch lacks a more specific follicular term in the retrieved descendants. Preserve the original human ISS and donor relation, and do not map mouse A/D labels onto human natural products. Proposed replacements: negative regulation of T-helper cell differentiation Supporting Evidence: |
| GO:0071356 cellular response to tumor necrosis factor | IEA GO_REF:0000107 | UNDECIDED | Summary: The TNF-response transfer has expression/localization evidence but unresolved FOXP1-specific participation. Reason: Original PMID26842647 Methods/Results and Fig2–3 captions were read. Primary rat cortical neurons receive human recombinant TNF and XPO1 inhibitors; FOXP1 immunofluorescence changes alongside AKT and NF-kappaB. Nuclear FOXP1 also increases in treated rat injury models. These establish expression/localization responses, but the intervention targets nuclear export rather than FOXP1 and does not isolate its contribution to protection. Preserve the human electronic transfer and donor IEP scope without asserting a curation error. Supporting Evidence: |
| GO:1900424 regulation of defense response to bacterium | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: Retain a contextual role in regulating antibacterial defense. Reason: Original PMID18799727 human-FOXP1 transgenic mice have reduced macrophage accumulation, bacterial clearance and survival in the tested peritonitis model, with macrophage functional defects. These support the existing regulatory defense context as non-core. FOXP1 is not thereby assigned direct antibacterial chemistry, and mouse-host effects are distinguished from a direct human clinical infection assay. Supporting Evidence: |
| GO:1901256 regulation of macrophage colony-stimulating factor production | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | KEEP AS NON CORE | Summary: The source measures M-CSF production separately from c-Fms receptor regulation. Reason: Original PMID18799727 Table3 reports reduced M-CSF in LPS-stimulated human-FOXP1-transgenic mouse macrophages. This supports the non-core cytokine-production regulation term. The measured M-CSF ligand endpoint is kept distinct from repression/rescue of its c-Fms/M-CSFR receptor; direct binding to a cytokine promoter is not established by these results. Supporting Evidence: |
| GO:1901300 positive regulation of hydrogen peroxide-mediated programmed cell death | IEA GO_REF:0000107 | UNDECIDED | Summary: The hydrogen-peroxide survival result is positive, but its programmed-death endpoint remains unresolved. Reason: Original PMID26333362 main Results explicitly report increased H2O2 survival after Foxp1 knockdown, referring to unread Online FigVIII G. The inspected caspase and PI assays use chelerythrine. Preserve the rat IMP transfer while resolving the H2O2-specific programmed-death readout; do not substitute the distinct stimulus or infer an error from unavailable supplemental detail. Supporting Evidence: |
| GO:1901509 regulation of endothelial tube morphogenesis | IMP PMID:24023716 FoxP1 stimulates angiogenesis by repressing the inhibitory g... | KEEP AS NON CORE | Summary: FOXP1 regulates endothelial tube formation in the tested human cell model. Reason: Original PMID24023716 HUVEC knockdown and overexpression alter Matrigel tube-formation phenotypes. Keep this non-core morphogenesis context, distinct from a mature perfused-vessel assay or direct SEMA5B binding. Human transcript identity is given, but protein-size wording is not used to assign a current natural product. Supporting Evidence: |
| GO:1990837 sequence-specific double-stranded DNA binding | IDA PMID:28473536 Impact of cytosine methylation on DNA binding specificities ... | TOO GENERAL | Summary: The directly measured DNA-binding specificity is represented more precisely by the existing cis-regulatory term. Reason: The original PMID28473536 S1/S2 workbook explicitly contains human FOXP1 eDBD, exact canonical residues288–576, and both HT-SELEX and methyl-HT-SELEX motifs. This is genuine FOXP1 evidence; it is not a full-length or unique-product assay. GO:0000978 is an is_a descendant of sequence-specific double-stranded DNA binding and is independently supported by human promoter experiments. No methylation-insensitive class or equal affinity is inferred from the common motif. |
| GO:2000341 regulation of chemokine (C-X-C motif) ligand 2 production | IDA PMID:18799727 Down-regulation of the forkhead transcription factor Foxp1 i... | UNDECIDED | Summary: The exact CXCL2-production endpoint has not been verified. Reason: The inspected PMID18799727 Table3 measures MCP-1/CCL2, which is not CXCL2, and Table2 concerns F4/80/Mac-3 tissue content. The selected indexed main-text search did not recover CXCL2/MIP-2; supplements were not inspected. Preserve this experimental annotation as undecided rather than concluding that the paper lacks the endpoint or is miscited. Other supported cytokine effects do not substitute for the exact chemokine. Supporting Evidence: |
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Download this section (compressed HTML)Q: Which endogenous human targets are differentially recognized and regulated by canonical FOXP1 and FOXP1-ES, and how much of the difference reflects DNA specificity versus partner recruitment?
Q: When does SMRT recruitment dominate FOXP1 regulation, and when do FOXP2, FOXP4, androgen receptor or other partners alter the direction of transcriptional output?
Q: Is the restraint of IL21 and follicular-helper differentiation observed in mouse T cells conserved in matched human T-cell states?
Q: Which FOXP1-dependent transcriptional changes account for the contrasting survival effects in human B cells and rodent cardiomyocytes?
Experiment: Use endogenous isoform-selective perturbations and matched rescue in human stem-cell differentiation, combining sequence-verified constructs, nascent RNA, occupancy and partner-association measurements. Distinguish shared antibody signals from isoform-specific occupancy.
Experiment: Perturb endogenous FOXP1 partners in matched human cell contexts while measuring occupancy, transcription and reciprocal complex recovery. Interface tests should distinguish cellular association from direct contact.
Experiment: Measure IL21, ICOS and follicular-helper maturation after controlled FOXP1 perturbation in a human T-cell differentiation system, with matched state and activation controls.
Experiment: Compare early transcriptional changes and later survival endpoints after matched FOXP1 perturbation in human B cells and a validated human cardiomyocyte model, separating stimulus identity, growth and proliferation.
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