ARID1B (BAF250B/p250R) is a nuclear DNA-binding and assembly subunit of canonical mammalian SWI/SNF chromatin-remodeling complexes. Its ARID region binds DNA without an established sequence preference, and other regions associate with the SMARCA2 or SMARCA4 ATPase and additional complex subunits. ARID1B and ARID1A are mutually exclusive alternatives in these assemblies, coupling DNA engagement and regulatory recruitment to ATP-dependent nucleosome remodeling. Human ARID1B also supports steroid-receptor transcriptional coactivation in tested cellular contexts. ARID1B-dependent gene regulation is important in development, and pathogenic loss of function causes Coffin–Siris syndrome.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000785 chromatin | NAS PMID:12192000 REST repression of neuronal genes requires components of the... | ACCEPT | Summary: ARID1B engages chromatin within human SWI/SNF assemblies. Reason: Chromatin is consistent with ARID1B's directly demonstrated DNA binding and human SWI/SNF-A membership in PMID:15170388 and 12200431. The REST/CoREST source does not expose its exact ARID1B experiment in the inspected abstract; this broad location is retained with independent target support and that source gap explicit. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: PMID:15170388 Analysis of DNA-binding behaviour indicates that ARID1B binds DNA in a non-sequence-specific manner similar to p270. PMID:12200431 Mass spectrometric analysis, and immunoblotting with antibodies specific to hOsa1 or hOsa2 demonstrate the presence of both proteins in SWI/SNF-A but not in the related polybromo-BRG1-associated factors complex purified from HeLa cells. |
| GO:0003677 DNA binding | IDA PMID:15170388 Two related ARID family proteins are alternative subunits of... | ACCEPT | Summary: Human ARID1B binds DNA without evident sequence specificity. Reason: Actual PMID:15170388 Methods and Figures 7–8 test recombinant human ARID1B DNA association and show no evident sequence selectivity. This supports DNA binding without inferring AT-rich preference from the ARID domain name. Supporting Evidence: PMID:15170388 Analysis of DNA-binding behaviour indicates that ARID1B binds DNA in a non-sequence-specific manner similar to p270. |
| GO:0003677 DNA binding | IEA GO_REF:0000002 | ACCEPT | Summary: The ARID-domain DNA-binding inference agrees with direct target assays. Reason: The original InterPro domain mappings agree with direct human ARID1B DNA-binding assays in PMID:15170388. Retain the broad activity; the exact mapping-rule derivation is not independently reconstructed and no sequence preference is added. Supporting Evidence: PMID:15170388 Analysis of DNA-binding behaviour indicates that ARID1B binds DNA in a non-sequence-specific manner similar to p270. |
| GO:0003713 transcription coactivator activity | NAS PMID:11734557 SYT associates with human SNF/SWI complexes and the C-termin... | ACCEPT | Summary: Human hOsa2/ARID1B supports steroid-receptor transcriptional coactivation. Reason: The original p250R source identifies a human SNF/SWI component but its individual coactivation assay remains unread. Independent actual human hOsa2 steroid-receptor reporter experiments in PMID:12200431 establish this same broad function; the inspected 11734557 erratum changes funding and peptide numbering, not the biological conclusion. The seeded NAS record was assigned by UniProt using ECO:0000303 on 20031216; its original reference is preserved. Supporting Evidence: PMID:12200431 In cultured mammalian cells, hOsa1 and hOsa2 stimulate transcription by the glucocorticoid, estrogen, and androgen receptors. |
| GO:0005515 protein binding | IPI PMID:12200431 Largest subunits of the human SWI/SNF chromatin-remodeling c... | MODIFY | Summary: Human ARID1B associates with the SMARCA2 ATPase. Reason: Own-source PMID:12200431 identifies human hOsa2 association with hBRM/SMARCA2 using reciprocal C33A co-IP and GST-hOsa2/in-vitro-translated partner assays. ATPase binding is more informative than generic protein binding. Preserve partner P51531 and the original IPI provenance; no autonomous ARID1B ATPase activity is asserted. Proposed replacements: ATPase binding Supporting Evidence: PMID:12200431 Co-precipitation studies indicate that hOsa1 and hOsa2 associate with BRG1 and hBRM through the C-terminal domain of hOsa. |
| GO:0005515 protein binding | IPI PMID:12200431 Largest subunits of the human SWI/SNF chromatin-remodeling c... | MODIFY | Summary: Human ARID1B associates with the SMARCA4 ATPase. Reason: Own-source PMID:12200431 resolves hOsa2 association with BRG1/SMARCA4 in reciprocal cellular and domain-binding experiments. Refine to ATPase binding while preserving P51532 and the original evidence. GST bait and translated partner fragments are distinguished from two purified full-length proteins. Proposed replacements: ATPase binding Supporting Evidence: PMID:12200431 Co-precipitation studies indicate that hOsa1 and hOsa2 associate with BRG1 and hBRM through the C-terminal domain of hOsa. |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | UNDECIDED | Summary: The exact BioPlex ARID1B–SMARCC2 assay remains uninspected. Reason: The BioPlex platform is read, but the exact ARID1B–SMARCC2 record, bait and confidence evidence from PMID:33961781 remain uninspected. Established BAF membership does not reconstruct this particular IPI assay or justify removing it. |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | UNDECIDED | Summary: The exact OpenCell ARID1B–SMARCA4 assay remains unresolved. Reason: The OpenCell ARID1B–SMARCA4 target pair and its underlying experiment have not been inspected. Independent human BRG1 association is real, but cannot supply source-local assay details or a refinement to this screen assertion. |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | UNDECIDED | Summary: The OpenCell ARID1B–SMARCC2 pair requires its target record. Reason: The exact OpenCell ARID1B–SMARCC2 pair record remains unread. Preserve the positive curated IPI source without claiming that platform-level methods resolve this association. |
| GO:0005515 protein binding | IPI PMID:36950384 Protein interaction studies in human induced neurons indicat... | UNDECIDED | Summary: The neuronal ARID1B–SMARCA2 result needs source-local verification. Reason: The neuron-specific interactome's exact ARID1B–SMARCA2 result remains uninspected. ARID1B antibodies occur in the actual resource list, but reagent presence is not the target pair result. |
| GO:0005515 protein binding | IPI PMID:36950384 Protein interaction studies in human induced neurons indicat... | UNDECIDED | Summary: The neuronal ARID1B–SMARCA4 result needs source-local verification. Reason: The PMID:36950384 ARID1B–SMARCA4 pair result and its neuronal context remain unresolved in the inspected text. Earlier human BRG1 binding supports biology but does not close this source's individual experiment. |
| GO:0005515 protein binding | IPI PMID:36950384 Protein interaction studies in human induced neurons indicat... | UNDECIDED | Summary: The ARID1B–DPYSL2 network association remains source-limited. Reason: The exact ARID1B–DPYSL2 neuronal-network record remains unread. A positive UniProt interaction summary is acknowledged but does not establish the specific source assay, interface or function. |
| GO:0005515 protein binding | IPI PMID:36950384 Protein interaction studies in human induced neurons indicat... | UNDECIDED | Summary: The neuronal ARID1B–SMARCC2 assay remains uninspected. Reason: The ARID1B–SMARCC2 association attributed to PMID:36950384 requires its target table or figure. Native BAF assembly makes it plausible without validating this particular IPI record. |
| GO:0005515 protein binding | IPI PMID:40205054 Multimodal cell maps as a foundation for structural and func... | UNDECIDED | Summary: The newer ARID1B–SMARCC2 interaction record remains uninspected. Reason: The PMID:40205054 ARID1B–SMARCC2 interaction record was not inspected. Broad platform findings or the absence of a main-text target mention cannot adjudicate or refute an experimental pair annotation. |
| GO:0005634 nucleus | EXP PMID:11988099 Cloning and characterization of hELD/OSA1, a novel BRG1 inte... | ACCEPT | Summary: Independent human evidence supports the historical nuclear assignment. Reason: Historical hELD/OSA1 is mapped to ARID1B by the original 15170388 alias discussion and UniProt AF468300 provenance. The 11988099 localization assay itself remains unread, but independent human nuclear-complex recovery and supported HPA nucleoplasm localization corroborate the original nuclear EXP assertion. Supporting Evidence: PMID:12200431 Mass spectrometric analysis, and immunoblotting with antibodies specific to hOsa1 or hOsa2 demonstrate the presence of both proteins in SWI/SNF-A but not in the related polybromo-BRG1-associated factors complex purified from HeLa cells. file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. file:human/ARID1B/ARID1B-notes.md Historical hELD/OSA1 in PMID:11988099 is mapped to ARID1B by the alias discussion in PMID:15170388 and UniProt AF468300/AAL76077.1 provenance. Inoue hOsa1 is ARID1A, whereas Inoue hOsa2 is ARID1B; historical constructs are not assigned a modern isoform from the shared names. |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: Human ARID1B occupies a nuclear pool. Reason: UniProt's nuclear-location mapping agrees with native human nuclear ARID1B complexes and supported HPA nucleoplasm localization. The broad compartment is retained without an exclusivity claim. Supporting Evidence: PMID:12200431 Mass spectrometric analysis, and immunoblotting with antibodies specific to hOsa1 or hOsa2 demonstrate the presence of both proteins in SWI/SNF-A but not in the related polybromo-BRG1-associated factors complex purified from HeLa cells. file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. |
| GO:0005654 nucleoplasm | IBA GO_REF:0000033 | ACCEPT | Summary: Inherited nucleoplasmic localization has independent target support. Reason: The inherited nucleoplasmic assignment agrees with direct human HPA and native nuclear-complex evidence. PTN000291886 topology remains untraced; target self-inclusion is legitimate descendant evidence rather than circularity. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000291886 · PTN000291886 UNRESOLVED Original PAINT ancestral node retained. Complete topology, MSA and source assays were not reconstructed. Target self-inclusion and donor count are not defects; independent target evidence and specialized-complex limits are evaluated in the rationale. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: The Human Protein Atlas supports ARID1B nucleoplasmic localization. Reason: The current HPA target table reports supported nucleoplasm localization for human ARID1B. Uncertain plasma-membrane/cytosolic signals are not generalized, and images were not independently reinterpreted. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9825847 | ACCEPT | Summary: ARID1B has an independently supported nucleoplasmic transcriptional pool. Reason: The MITF/TYRP1 recruitment event places the curated ARID1B source in a nuclear transcriptional context. Its exact entity graph is uninspected, while independent human HPA and native nuclear-complex evidence support this broad nucleoplasmic location. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. Reactome:R-HSA-9825847 MITF-M binds to the promoter of the TYRP1 gene to stimulate expression as assessed by reporter gene assay, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) (Bertolotto et al, 1998a, b; Fang et al, 2002; De la Serna et al, 2006; reviewed in Cheli et al, 2010). Promoter recognition is mediated by an M-box (located between position -49 and -39 in human, -44 and -33 in mouse) and a related E-box (position -238 to -233 in mouse) (Bertolotto et al, 1998a; Fang et al, 2002). Expression is also stimulated by the MITF-M-dependent recruitment of a SWI/SNF complex as assessed by co-immunoprecipitation of SMARCA4 (BRG1), SMARCE1 (INI1) and SMARCB1 (BAF57) in mouse, and in an additional study with SMARCD1 (de la Serna et al, 2006; Keenen et al, 2010; Aras et al, 2019). |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9932437 | ACCEPT | Summary: ARID1B-containing cBAF assembly is consistent with nucleoplasmic localization. Reason: The actual event explicitly distinguishes ARID1A- and ARID1B-containing cBAF assembly and DNA/ATPase contacts. Independent human localization supports its nucleoplasmic pool; ARID1B is not assigned ATP hydrolysis. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. Reactome:R-HSA-9932437 Recruitment of ARID1A or ARID1B to the forming cBAF complex represent a branching point that distinguishes it from pBAF, which contains ARID2 (Mashtalir et al, 2018; Mashtalir et al, 2020; He et al, 2020; Euskirchen et al, 2012). ARID1A and ARID1B extensively cross-link with core components of the assembling complex including SMARCC, SMARCD, SMARCB1 and SMARCE1 (Mashtalir et al, 2018). The ARID subunit in turn is responsible for making many of the contacts with the catalytic ATPase module as well as non-specifically with DNA (Mashtalir et al, 2018; Mashtalir et al 2020; reviewed in Euskirchen et al, 2012). <br>The functions of ARID1A- versus ARID1B -containing complexes are overlapping yet distinct, with both shared and unique genomic targets and different expression patterns. ARID1A expression is high in embryonic stem cells and ARID1B expression is activated during differentiation (Staahl et al, 2013; Staahl and Crabtree, 2013; Raab et al, 2015; reviewed in Pagliaroli and Trizzino, 2021). ARID1A and ARID1B are highly mutated in many cancers and in a range of neurodevelopmental disorders (reviewed in Bogershausen and Wollnick, 2018; Pagliaroli and Trizzino, 2021; Cenik and Shilatifard, 2021; Wang and Tang, 2023) |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9932836 | ACCEPT | Summary: DPF recruitment occurs within an ARID-containing nuclear assembly. Reason: The event describes DPF recruitment to the ARID/SMARCC-containing cBAF core. The broad nuclear location is independently supported; DPF's histone-reading activity is not transferred to ARID1B and the full entity graph remains uninspected. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. Reactome:R-HSA-9932836 cBAF assembly continues with the addition of a DPF protein (Double PHD Finger), a defining constituent of the complex (Mashtalir et al, 2018; Mashtalir et al, 2020). Three mutually exclusive DPF proteins may form part of the cBAF complex, DPF1 (also known as BAF45B), DPF2 (BAF45D) or DPF3 (BAF45C). The DPF subunit forms part of the base module of the SWI/SNF complex that contacts the nucleosome, and DPF proteins are recruited through interaction with ARID and SMARCC proteins (He et al, 2020). DPF proteins bind to acetylated tails of histone H3 and H4 (Hyun et al, 2024; Lange et al, 2008; Huber et al, 2017). Selective incorporation of DPF1, 2 or 3 in the cBAF complex may reflect cell type specificity or stage in development (Lange et al, 2008 Lessard et al, 2007). |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9933238 | ACCEPT | Summary: The ARID-containing core joins an ATPase module in the nuclear pool. Reason: The event joins the SS18-associated ATPase module to an ARID-containing core. This agrees with ARID1B's established nucleoplasmic assembly, without treating complex assembly as an independent localization experiment. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. Reactome:R-HSA-9933238 Isolation of SMARC4A-containing complexes suggests that the ATPase module of cBAF, pBAF and ncBAF complexes exist as discrete, isolatable complexes. The ATPase modules of cBAF and ncBAF are the same, and consist of SMARCA2/4, a dimer of ACTB and ACTL6A/B (which together form the actin-related protein or ARP module linking the catalytic core of the SWI/SNF complex to the core/base module), the BCL7 proteins and SS18 (Kadoch et al, 2013; Mashtalir et al, 2018; Mashtalir et al, 2020; He et al, 2020; reviewed in Eustermann et al, 2024). |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9934021 | ACCEPT | Summary: Curated npBAF assembly agrees with independently supported human nucleoplasm. Reason: The npBAF summary explicitly includes ARID1A or ARID1B while retaining a mouse experimental basis. Human HPA independently supports the broad nucleoplasmic annotation; no new human neural-assembly assay is inferred. Supporting Evidence: file:human/ARID1B/ARID1B-notes.md The inspected Human Protein Atlas ARID1B table reports supported nucleoplasm localization; plasma-membrane and cytosolic signals are uncertain. This supports a human nuclear pool without assigning exclusive localization or reinterpreting image pixels. Reactome:R-HSA-9934021 Studies in mice identified a neural progenitor (np) BAF complex that is required for the proliferation of neural stem and progenitor cells (Lessard et al, 2007; Staahl et al, 2013). These complexes differ slightly from esBAF complexes in subunit composition. npBAF complexes contain either SMARCA4 or SMARCA2 as catalytic subunits, may contain either ARID1A or ARID1B, and contain SMARCD1 and SMARCD3 but not SMARCD2 (Lessard et al, 2007; Stahl et al, 2013; reviewed in Staahl and Crabtree, 2013; Kadoch and Crabtree, 2015; Cenik and Shilatifard, 2021; Innis and Cabot, 2020). |
| GO:0006338 chromatin remodeling | IEA GO_REF:0000002 | ACCEPT | Summary: ARID1B contributes to chromatin remodeling through DNA and assembly contacts. Reason: The IPR021906 remodeling mapping is consistent with ARID1B's DNA-binding and ATPase-associated structural role in human cBAF. It contributes to complex remodeling rather than hydrolyzing ATP itself; exact electronic-rule reconstruction is unresolved. Supporting Evidence: Reactome:R-HSA-9932437 The ARID subunit in turn is responsible for making many of the contacts with the catalytic ATPase module as well as non-specifically with DNA |
| GO:0006338 chromatin remodeling | NAS PMID:10078207 Reconstitution of a core chromatin remodeling complex from S... | ACCEPT | Summary: Human ARID1B contributes to the broad remodeling activity of its complex. Reason: The original minimal reconstitution centers on BRG1 and other core subunits, so it is not presented as an isolated ARID1B assay. Independent human ARID1B assembly/DNA evidence establishes its contribution to the same broad remodeling process and supports retention of this NAS assertion with that source limitation. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: Reactome:R-HSA-9932437 The ARID subunit in turn is responsible for making many of the contacts with the catalytic ATPase module as well as non-specifically with DNA PMID:15170388 Immunocomplex analysis provides direct evidence that endogenous ARID1B is associated with SWI/SNF-related complexes and indicates that p270 and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes. |
| GO:0006357 regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: Human target evidence supports inherited Pol II transcriptional regulation. Reason: Human hOsa2 coactivation and chromatin-complex participation corroborate inherited regulation of PolII transcription. The actual PTN000291886 placement is untraced; neither the donor count nor target self-support is used against the IBA. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000291886 · PTN000291886 UNRESOLVED Original PAINT ancestral node retained. Complete topology, MSA and source assays were not reconstructed. Target self-inclusion and donor count are not defects; independent target evidence and specialized-complex limits are evaluated in the rationale. Supporting Evidence: PMID:12200431 In cultured mammalian cells, hOsa1 and hOsa2 stimulate transcription by the glucocorticoid, estrogen, and androgen receptors. |
| GO:0006357 regulation of transcription by RNA polymerase II | NAS PMID:11263494 The murine SNF5/INI1 chromatin remodeling factor is essentia... | ACCEPT | Summary: The broad Pol II regulatory role is independently supported in human cells. Reason: The cited source studies murine SNF5/INI1, and its precise ARID1B derivation is unresolved. The same broad transcriptional role is independently established by human hOsa2 reporter and complex studies; acceptance does not relabel the original mouse perturbation as a human ARID1B experiment. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: PMID:12200431 In cultured mammalian cells, hOsa1 and hOsa2 stimulate transcription by the glucocorticoid, estrogen, and androgen receptors. |
| GO:0006357 regulation of transcription by RNA polymerase II | NAS PMID:17340523 Separation and Quantification of Some Alkaloids from Fumaria... | UNDECIDED | Summary: The original transcriptional assertion has a verified unrelated PMID. Reason: Official PubMed17340523 resolves to Fumaria alkaloid separation. Preserve the original reference and flag WRONG_IDENTIFIER with no guessed replacement; independent transcriptional biology does not repair this verified citation defect. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. |
| GO:0006357 regulation of transcription by RNA polymerase II | NAS PMID:17920018 Regulation of dendritic development by neuron-specific chrom... | ACCEPT | Summary: Independent human evidence supports broad Pol II regulation. Reason: The source emphasizes BAF53b-dependent neuronal transcription, with exact ARID1B-specific evidence untraced. Retain the broad PolII-regulatory function on independent human hOsa2 evidence while keeping this original NAS derivation unresolved. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: PMID:12200431 In cultured mammalian cells, hOsa1 and hOsa2 stimulate transcription by the glucocorticoid, estrogen, and androgen receptors. |
| GO:0016514 SWI/SNF complex | IBA GO_REF:0000033 | ACCEPT | Summary: Human ARID1B is a SWI/SNF subunit. Reason: Human ARID1B-specific antibodies, native complex IP and hOsa2 purification directly corroborate inherited SWI/SNF membership. The exact PTN000291886 node is untraced, and legitimate target descendant evidence is retained. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000291886 · PTN000291886 UNRESOLVED Original PAINT ancestral node retained. Complete topology, MSA and source assays were not reconstructed. Target self-inclusion and donor count are not defects; independent target evidence and specialized-complex limits are evaluated in the rationale. Supporting Evidence: PMID:15170388 Immunocomplex analysis provides direct evidence that endogenous ARID1B is associated with SWI/SNF-related complexes and indicates that p270 and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes. |
| GO:0016514 SWI/SNF complex | IDA PMID:11734557 SYT associates with human SNF/SWI complexes and the C-termin... | ACCEPT | Summary: Human p250R/ARID1B occurs in native SWI/SNF complexes. Reason: The original complete abstract explicitly identifies p250R as a newly identified large subunit of native human SNF/SWI complexes; actual human ARID1B antibodies and hOsa2 purification independently confirm membership. SSX1's histone-binding result is not attributed to ARID1B, and the correction was inspected separately. Supporting Evidence: PMID:11734557 The SYT protein has a unique QPGY domain, which is also present in the largest subunits, p250 and the newly identified homolog p250R, of the corresponding SNF/SWI complexes. PMID:15170388 Immunocomplex analysis provides direct evidence that endogenous ARID1B is associated with SWI/SNF-related complexes and indicates that p270 and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes. |
| GO:0016514 SWI/SNF complex | IEA GO_REF:0000120 | ACCEPT | Summary: Electronic SWI/SNF membership agrees with direct human complex recovery. Reason: The combined ARBA/InterPro membership assertion agrees with direct human ARID1B isolation and alternative ARID1A/ARID1B complexes. Exact electronic derivation remains uninspected, but the target membership is established. Supporting Evidence: PMID:15170388 Immunocomplex analysis provides direct evidence that endogenous ARID1B is associated with SWI/SNF-related complexes and indicates that p270 and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes. |
| GO:0016514 SWI/SNF complex | NAS PMID:8804307 Diversity and specialization of mammalian SWI/SNF complexes. | ACCEPT | Summary: Later target-specific evidence supports the broad historical BAF membership. Reason: The early source describes heterogeneous mammalian BAF assemblies without resolving every modern 250 kDa identity in its abstract. Independent human p250R/hOsa2/ARID1B evidence establishes the same SWI/SNF membership; no specific early band is retroactively assigned an isoform. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: PMID:15170388 Immunocomplex analysis provides direct evidence that endogenous ARID1B is associated with SWI/SNF-related complexes and indicates that p270 and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes. |
| GO:0030071 regulation of mitotic metaphase/anaphase transition | NAS PMID:23698369 BAF complexes facilitate decatenation of DNA by topoisomeras... | UNDECIDED | Summary: ARID1B participation in the metaphase/anaphase transition remains unresolved. Reason: Actual PMID:23698369 includes BAF250b antibodies, so a categorical absence or paralog error is unwarranted. The inspected mapped TOP2A/decatenation mechanism and perturbation are resolved for BAF250a; the ARID1B-specific metaphase/anaphase role remains uncertain. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Complex participation can support this process without isolated subunit activity; the unresolved point is which ARID1B-containing assembly underlies the specific transition claim. |
| GO:0031491 nucleosome binding | IBA GO_REF:0000033 | ACCEPT | Summary: ARID1B contributes to cooperative nucleosome engagement by its complex. Reason: The original IBA explicitly records contribution to nucleosome binding. ARID1B's demonstrated DNA binding and contacts within the substrate-engaging remodeling complex support that cooperative role without claiming an isolated histone-binding interface. Exact PTN000291886/experimental-node placement remains unresolved. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000291886 · PTN000291886 UNRESOLVED Original PAINT ancestral node retained. Complete topology, MSA and source assays were not reconstructed. Target self-inclusion and donor count are not defects; independent target evidence and specialized-complex limits are evaluated in the rationale. Supporting Evidence: PMID:15170388 Analysis of DNA-binding behaviour indicates that ARID1B binds DNA in a non-sequence-specific manner similar to p270. Reactome:R-HSA-9932437 The ARID subunit in turn is responsible for making many of the contacts with the catalytic ATPase module as well as non-specifically with DNA |
| GO:0035060 brahma complex | IEA GO_REF:0000002 | ACCEPT | Summary: Human ARID1B associates with BRM-containing complexes. Reason: The current brahma-complex definition includes mammalian BRM-containing SWI/SNF. Direct native and recombinant human hOsa2/ARID1B–BRM association supports the IPR021906 inference; this term is not restricted to Drosophila. Supporting Evidence: PMID:15170388 The ARID-containing subunits are not specific to the ATPases. Each associates with both BRG1 and hBRM, thus increasing the number of distinct subunit combinations known to be present in cells. |
| GO:0035060 brahma complex | NAS PMID:8804307 Diversity and specialization of mammalian SWI/SNF complexes. | ACCEPT | Summary: Human target evidence corroborates the historical BRM-complex assignment. Reason: Although the 1996 abstract does not resolve its modern ARID1B/BRM identity chain, later direct human BRM association in 12200431 and 15170388 supports this same established membership. Preserve the NAS provenance and its unresolved historical experiment. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: PMID:15170388 The ARID-containing subunits are not specific to the ATPases. Each associates with both BRG1 and hBRM, thus increasing the number of distinct subunit combinations known to be present in cells. |
| GO:0045582 positive regulation of T cell differentiation | NAS PMID:12110891 Reciprocal regulation of CD4/CD8 expression by SWI/SNF-like ... | UNDECIDED | Summary: The relevant ARID1B-containing T-cell differentiation assembly is unresolved. Reason: The available T-cell study resolves Brg/BAF57 perturbations, not the ARID1B-specific mechanism underlying this NAS row. Broad BAF membership does not independently close positive T-cell differentiation; no incorrect-experiment claim is made. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. The gap is the relevant ARID1B-containing T-cell assembly and curator derivation, not a requirement for purified or isolated subunit activity. |
| GO:0045597 positive regulation of cell differentiation | NAS PMID:11790558 SWI/SNF chromatin remodeling and cancer. | UNDECIDED | Summary: The specific positive differentiation context remains unresolved. Reason: The general remodeling/cancer source does not expose the ARID1B-specific positive differentiation evidence. The particular process assertion remains unresolved despite the established broad transcriptional function. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. A subunit can participate through its complex; the relevant ARID1B-containing variant and positive differentiation context remain unresolved. |
| GO:0045597 positive regulation of cell differentiation | NAS PMID:12368262 Identification of a polymorphic, neuron-specific chromatin r... | UNDECIDED | Summary: Historical neuronal assembly does not resolve the positive differentiation assertion. Reason: The available neuronal-complex Discussion treats BAF250a/b combinatorial assembly as an assumption. The relevant ARID1B-containing assembly and positive differentiation context have not been resolved in the inspected source scope. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. The source-specific gap is the relevant ARID1B-containing neuronal assembly and positive differentiation context, not whether an isolated subunit catalyzes the process. |
| GO:0045663 positive regulation of myoblast differentiation | NAS PMID:11175787 Mammalian SWI/SNF complexes promote MyoD-mediated muscle dif... | UNDECIDED | Summary: The relevant ARID1B-containing myogenic assembly remains unresolved. Reason: The MyoD study's abstract describes BRG1/BRM-dependent myogenic remodeling. The relevant ARID1B-containing assembly, myoblast context and ComplexPortal curator derivation remain untraced. A subunit can contribute within its complex; isolated subunit activity is not required. The original ComplexPortal NAS assertion (ECO:0005547, 20251211) and PMID:11175787 are preserved. |
| GO:0045815 transcription initiation-coupled chromatin remodeling | NAS PMID:11734557 SYT associates with human SNF/SWI complexes and the C-termin... | UNDECIDED | Summary: Expression-permissive initiation-coupled remodeling remains source-limited. Reason: The current GO definition describes epigenetic remodeling that makes chromatin permissive for expression and relates it to initiation; it is not restricted to one kinetic assay. The inspected original abstract identifies p250R in human complexes but does not resolve this specific ARID1B activity. Independent DNA/assembly contacts and receptor-reporter effects do not close that chromatin mechanism. Retain the original UniProt NAS assertion as uncertain without claiming it false. Remove the redundant child from the core, retaining established broad remodeling. The seeded NAS record was assigned by UniProt using ECO:0000303 on 20031216; its original reference is preserved. |
| GO:0045893 positive regulation of DNA-templated transcription | IBA GO_REF:0000033 | ACCEPT | Summary: Human receptor reporters support positive transcriptional regulation. Reason: The inherited positive-transcription assertion is independently corroborated by direct human hOsa2 steroid-receptor reporter experiments. The source node is retained with topology unresolved; no species-general receptor specificity is inferred. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000291886 · PTN000291886 UNRESOLVED Original PAINT ancestral node retained. Complete topology, MSA and source assays were not reconstructed. Target self-inclusion and donor count are not defects; independent target evidence and specialized-complex limits are evaluated in the rationale. Supporting Evidence: PMID:12200431 In cultured mammalian cells, hOsa1 and hOsa2 stimulate transcription by the glucocorticoid, estrogen, and androgen receptors. |
| GO:0070316 regulation of G0 to G1 transition | NAS PMID:11790558 SWI/SNF chromatin remodeling and cancer. | UNDECIDED | Summary: ARID1B-dependent G0-to-G1 control remains source-limited. Reason: The source is a broad SWI/SNF/cancer review and the particular ARID1B control of G0-to-G1 transition is not resolved. This uncertainty is distinct from accepted general transcriptional regulation. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. An ARID1B-containing complex could perform the regulatory work; the specific G0-to-G1 context and curator reconstruction are untraced. |
| GO:0071564 npBAF complex | NAS PMID:8804307 Diversity and specialization of mammalian SWI/SNF complexes. | ACCEPT | Summary: Curated target-specific assembly supports npBAF membership. Reason: Accept npBAF membership using the independently inspected human Reactome ARID1B entity tree, cached R-HSA-9934021 and current UniProt subunit statement. These are curated assemblies with a mouse/orthology basis, not newly observed human biochemical isolation. Preserve original ComplexPortal NAS/8804307 provenance without claiming its historical target-specific experiment was reread. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: Reactome:R-HSA-9934021 npBAF complexes contain either SMARCA4 or SMARCA2 as catalytic subunits, may contain either ARID1A or ARID1B, and contain SMARCD1 and SMARCD3 but not SMARCD2 file:human/ARID1B/ARID1B-uniprot.txt Component of neural progenitors-specific chromatin remodeling complex CC (npBAF complex) composed of at least, ARID1A/BAF250A or ARID1B/BAF250B, CC SMARCD1/BAF60A, SMARCD3/BAF60C, SMARCA2/BRM/BAF190B, CC SMARCA4/BRG1/BAF190A, SMARCB1/BAF47, SMARCC1/BAF155, SMARCE1/BAF57, CC SMARCC2/BAF170, PHF10/BAF45A, ACTL6A/BAF53A and actin. |
| GO:0071565 nBAF complex | IBA GO_REF:0000033 | ACCEPT | Summary: Curated target-specific assembly supports nBAF membership independently of untraced ancestry. Reason: Accept nBAF membership using the independently inspected human Reactome ARID1B entity tree and current UniProt subunit statement, consistent with the current official GO definition. Preserve PTN002652024 as untraced ancestry; independent biological corroboration resolves membership without claiming the tree/MSA was reconstructed or using donor count as evidence. Propagation Review Root cause: UNRESOLVED Sources checked: PANTHER:PTN002652024 · PTN002652024 UNRESOLVED Original PTN002652024 retained; complete topology, MSA and source experiments remain untraced. Target-specific curated human nBAF membership independently supports acceptance. No donor-count or self-support objection is made. Supporting Evidence: file:human/ARID1B/ARID1B-uniprot.txt Component of CC neuron-specific chromatin remodeling complex (nBAF complex) composed of CC at least, ARID1A/BAF250A or ARID1B/BAF250B, SMARCD1/BAF60A, CC SMARCD3/BAF60C, SMARCA2/BRM/BAF190B, SMARCA4/BRG1/BAF190A, CC SMARCB1/BAF47, SMARCC1/BAF155, SMARCE1/BAF57, SMARCC2/BAF170, CC DPF1/BAF45B, DPF3/BAF45C, ACTL6B/BAF53B and actin (By similarity). |
| GO:0071565 nBAF complex | NAS PMID:17920018 Regulation of dendritic development by neuron-specific chrom... | ACCEPT | Summary: Curated target-specific evidence supports mature neuronal BAF membership. Reason: Accept nBAF membership with the same independent curated target-specific assembly corroboration. Preserve original ComplexPortal NAS/17920018 provenance and the original BAF53b-focused experimental scope. This is a biological synthesis, not a newly inspected ARID1B assay in that paper. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Supporting Evidence: file:human/ARID1B/ARID1B-uniprot.txt Component of CC neuron-specific chromatin remodeling complex (nBAF complex) composed of CC at least, ARID1A/BAF250A or ARID1B/BAF250B, SMARCD1/BAF60A, CC SMARCD3/BAF60C, SMARCA2/BRM/BAF190B, SMARCA4/BRG1/BAF190A, CC SMARCB1/BAF47, SMARCC1/BAF155, SMARCE1/BAF57, SMARCC2/BAF170, CC DPF1/BAF45B, DPF3/BAF45C, ACTL6B/BAF53B and actin (By similarity). |
| GO:0140092 bBAF complex | NAS PMID:12368262 Identification of a polymorphic, neuron-specific chromatin r... | UNDECIDED | Summary: The distinct historical bBAF assembly remains unresolved. Reason: Actual PMID:12368262 Discussion assumes BAF250a/b combinatorial incorporation because the proteins are present in neurons and explicitly notes difficulty demonstrating it. The precise ARID1B bBAF membership is unresolved in this inspected scope, not shown false. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Current GO:0140092 distinguishes bBAF from nBAF by composition, so independently corroborated nBAF membership does not automatically resolve this separate assembly. |
| GO:2000045 regulation of G1/S transition of mitotic cell cycle | NAS PMID:10778858 Exit from G1 and S phase of the cell cycle is regulated by r... | UNDECIDED | Summary: The phase-specific G1/S regulatory assertion remains unresolved. Reason: The Rb/HDAC/SWI-SNF cell-cycle abstract does not expose the ARID1B-specific G1/S regulatory experiment. Transcriptional coactivation alone does not close this phase-specific assertion. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. The unresolved scope is the relevant ARID1B-containing complex and phase-specific regulation, not a requirement for autonomous subunit activity. |
| GO:2000781 positive regulation of double-strand break repair | NAS PMID:16932743 Mammalian SWI/SNF complexes facilitate DNA double-strand bre... | UNDECIDED | Summary: The relevant ARID1B-containing DNA-repair assembly remains unresolved. Reason: The inspected original Results perturb BRG1/BRM in mouse cells and human HeLa and demonstrate complex-dependent gamma-H2AX/DSB repair. The specific ARID1B contribution underlying this NAS assertion is not resolved; the genuine complex phenotype is retained as context. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Subunit contribution within a repair-active complex can establish participation. The inspected perturbations do not identify which ARID-containing assembly supports this particular curated claim. |
| GO:2000819 regulation of nucleotide-excision repair | NAS PMID:12215535 The SWI/SNF chromatin-remodeling factor stimulates repair by... | UNDECIDED | Summary: The ARID1B-containing nucleotide-excision repair context remains unresolved. Reason: The source examines SWI/SNF stimulation of nucleotide-excision repair; the inspected abstract and previously documented yeast-remodeler/human-repair-factor context do not resolve a human ARID1B-specific regulatory step. Preserve the source and uncertainty, without a title-based removal or a new repair assertion. The seeded NAS record was assigned by ComplexPortal using ECO:0005547 on 20251211; its original reference is preserved. Complex-mediated participation is sufficient in principle; the unresolved point is the relevant ARID1B-containing assembly and the original process derivation. |
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Download this section (compressed HTML)Q: Which exact source records resolve the remaining ARID1B partner pairs and specialized neural BAF assemblies?
Q: Which verified reference should replace the unrelated PMID:17340523 in the original transcription-regulation assertion?
Q: How do defined ARID1B isoforms and alternative ARID1A/ARID1B assemblies differ in recruitment, remodeling and coactivation in matched human cells?
Experiment: Compare endogenously tagged ARID1B isoforms in human neural progenitors and differentiated neurons using quantitative complex purification and chromatin occupancy, distinguishing assembly composition from isolated molecular activity.
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