DPF2, also called BAF45d or REQ, is a nuclear histone reader and transcriptional coregulator associated with SWI/SNF chromatin-remodeling complexes. Its tandem PHD fingers recognize histone H3 and H4 tails, including strong recognition of H3K14 crotonylation, and support chromatin recruitment. Other regions associate with transcription factors and remodeling-complex subunits. DPF2 can support transcriptional activation or repression in different contexts, including RelB/p52-dependent transcription and control of myeloid differentiation. Pathogenic variants that disrupt its PHD fingers are associated with Coffin-Siris syndrome. Two annotated natural protein products differ substantially in their zinc-finger region; their functional equivalence is not established.
Definition: A histone reader activity that recognizes histone H3 bearing crotonylation at lysine 14.
Justification: Human DPF2 tandem PHD fingers directly recognize H3K14-crotonylated peptides, and designer H3K14-crotonylated nucleosomes enrich endogenous DPF2 from human nuclear extract. The bounded current ontology search did not identify a corresponding named histone-reader child. This proposal records the missing specificity without inventing an identifier or adding a redundant parent annotation. The existing histone-reader core remains appropriate because it integrates recognition of several histone forms.
Parent term: histone reader activity
Supporting Evidence:
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000122 negative regulation of transcription by RNA polymerase II | TAS PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | ACCEPT | Reason: DPF2 represses differentiation-associated transcription in the human myeloid context examined in this study. Histone-pocket mutations impair recruitment to target chromatin and relieve the differentiation block. This is a supported regulatory activity, not an assertion that DPF2 is uniformly repressive: independent RelB/p52 experiments demonstrate coactivation in another context. |
| GO:0000785 chromatin | HDA PMID:16217013 Heterogeneous nuclear ribonucleoprotein C1/C2, MeCP1, and SW... | ACCEPT | Reason: The human K562 chromatin-associated LARC preparation contained requiem/DPF2 identified by LC-MS/MS of a 45-kDa band. The authors lacked an anti-requiem antibody for independent Western confirmation, so this is proteomic complex association rather than a DPF2-specific DNA-binding assay. Independent histone-binding and recruitment experiments substantiate the chromatin pool. |
| GO:0000785 chromatin | IDA PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | ACCEPT | Reason: Human DPF2 histone-binding and cellular recruitment experiments directly support association with chromatin. The folded histone-pocket mutant loses recruitment without simply losing nuclear entry. Recognition and recruitment do not confer the remodeling ATPase activity on DPF2. Supporting Evidence: PMID:28533407 Blocking these interactions through targeted mutagenesis of DPF2 abolishes its recruitment to target chromatin regions |
| GO:0000785 chromatin | NAS PMID:12192000 REST repression of neuronal genes requires components of the... | ACCEPT | Reason: The cited REST/CoREST study provides a chromatin-remodeling complex context; its accessible abstract does not resolve a DPF2-specific assay. The chromatin claim itself is independently established by human DPF2 proteomic association and histone-dependent recruitment, so it is retained without attributing the REST interaction mechanism specifically to DPF2. |
| GO:0003712 transcription coregulator activity | IBA GO_REF:0000033 | ACCEPT | Reason: The current PTHR45888 tree places the sequence-authenticated DPF2 leaf beneath the literal PTN008700032 coregulator IBD. The fly donor records contain experimental coactivator evidence. Independently, human DPF2 links RelB/p52 with SWI/SNF and supports integrated-promoter transcription, while RUNX1-associated myeloid repression demonstrates context-dependent regulatory sign. The broad coregulator claim is appropriate. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN008700032 · PTN008700032 SUPPORTS TRANSFER Literal IBD and target descent verified in PTHR45888; the target MSA sequence exactly matches the 391-residue canonical product. |
| GO:0003714 transcription corepressor activity | TAS PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | ACCEPT | Reason: Full-length DPF2 associates with RUNX1 and supports repression in the tested human myeloid context; histone recognition is required for recruitment and inhibition of differentiation. The isolated PHD tandem does not reproduce the RUNX1 association, separating TF-associated regulation from histone recognition. This corepressor subactivity coexists with independently demonstrated coactivation. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | KEEP AS NON CORE | Reason: The exact human DPF2–LDOC1 pair is present in the sequence-authenticated binary interaction dataset. Repeated pairwise testing supports positive binding capacity; it does not establish a particular DPF2 regulatory mechanism. Retain the generic association as non-core under the project instruction for supported protein binding. The inspected LDOC1 record does not establish a more informative enzyme or transcription-factor partner class. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | MODIFY | Reason: The exact DPF2–LNX1 binary pair and both reference-sequence checksums are verified. LNX1 is an experimentally characterized E3 ubiquitin-protein ligase, matching the current definition of ubiquitin protein ligase binding. This specific descendant replaces generic enzyme binding; it does not assign ligase activity to DPF2 or establish regulation of LNX1 catalysis in native cells. Proposed replacements: ubiquitin protein ligase binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | KEEP AS NON CORE | Reason: The original co-immunoprecipitation identifies ACTL6A in the DPF2-associated SWI/SNF context. ACTL6A is a nuclear actin-related complex subunit; that identity alone should not turn this association into actin-filament binding by DPF2. Retain the positive complex-associated protein interaction as non-core. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | MODIFY | Reason: The source identifies full-length DPF2 association with RUNX1, a sequence-specific DNA-binding transcription factor. DNA-binding transcription factor binding is therefore a more informative partner class. The evidence is co-immunoprecipitation and differential full-length versus PHD-only association, not a purified affinity measurement or a resolved direct-contact interface. Proposed replacements: DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | KEEP AS NON CORE | Reason: SMARCC2/BAF170 is identified in DPF2-associated SWI/SNF complexes. This supports a positive protein association within the remodeling machinery, without resolving an isolated binary interface or assigning the ATPase activity of the complex to either partner. Retain as non-core binding; the integrated complex function is represented separately. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | KEEP AS NON CORE | Reason: SMARCC1/BAF155 is identified in the DPF2-associated SWI/SNF complex. Preserve the positive association without converting co-complex recovery into a separate DPF2 catalytic or assembly activity. The histone-reader and transcription-coregulator cores describe the supported functional context. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The literal HuRI pair identifies GOLGA6L9, with the deposited interaction record specifying a sufficient-binding region at partner residues 159–432. Reference-sequence ROGIDs match, but that does not make the experimental fragment a full natural product. Retain positive non-core binding without inferring a Golgi role for DPF2. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The exact HuRI partner is HSF2BP, with sequence/taxon authentication. HSF2BP is a recombination-associated protein that also interacts with a heat-shock transcription factor; its name does not make it a folding chaperone. Preserve the positive binary association as non-core, without transferring those other partner functions to DPF2. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: This independently reported HuRI DPF2–LDOC1 pair is positive and sequence-authenticated. The dataset uses pairwise retesting and sequence confirmation, but it does not define the physiological regulatory consequence of this pair. Retain supported generic binding as non-core. The inspected LDOC1 record does not establish a more informative enzyme or transcription-factor partner class. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | MODIFY | Reason: The exact sequence-authenticated partner is TXNDC12, an endoplasmic-reticulum protein-disulfide oxidoreductase. The binary interaction supports enzyme binding as a partner-class refinement. It does not establish a physiological ER pool, redox activity or substrate relationship for DPF2. Proposed replacements: enzyme binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | MODIFY | Reason: The imported partner is MEOX2 accession Q6FHY5, a 303-residue sequence authenticated against its IntAct ROGID. Comparison with reviewed P50222 shows one upstream glutamine deletion and an identical homeobox DNA-binding region. Binding to this DNA-binding transcription-factor class is supported; the source accession is preserved, and neither a native target promoter nor transcriptional regulation by this isolated pair is inferred. Proposed replacements: DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The exact HuRI pair is DPF2–RINT1 and the reference sequences match the deposited checksums. Retain the positive binary association as non-core. RINT1 membrane-traffic and checkpoint functions do not by themselves define a corresponding mechanism or compartment for DPF2. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The literal TTC23L pair is present in the validated binary dataset and sequence-authenticated; the record includes the tagged interaction constructs. A more informative functional partner class was not established from the official TTC23L record. Keep the positive generic interaction as non-core. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The exact binary partner is ZNF655. Its official record describes a probable transcription factor, but the inspected evidence does not independently establish sequence-specific DNA recognition for the tested participant. Preserve positive binding as non-core rather than deriving a definitive DNA-binding transcription-factor class solely from a zinc-finger name. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The sequence-authenticated HuRI pair identifies RUBCN. This supports a positive association but does not show that DPF2 participates in autophagosome regulation or inherits RUBCN membrane-associated functions. Keep the generic binding observation as non-core. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Reason: The literal HuRI pair identifies PICK1 and both reference sequences match. Preserve its positive binary binding capacity as non-core; this result does not establish a DPF2 signaling-adaptor activity or connect the contact to its chromatin-regulatory mechanism. No compartment mismatch is used to reject the interaction. Supporting Evidence: |
| GO:0005634 nucleus | EXP PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | MODIFY | Reason: The source reports experimental nuclear localization of human DPF2. Refine the broad nuclear claim to the independently supported nucleoplasm and chromatin pools. This is nonexclusive target-level resolution using HPA and human chromatin-recruitment evidence, not a claim that the original assay separately visualized both pools or that chromatin has a nucleus ancestry edge. Proposed replacements: nucleoplasm chromatin |
| GO:0005634 nucleus | IDA PMID:29429572 Mutations in the BAF-Complex Subunit DPF2 Are Associated wit... | MODIFY | Reason: The source shows diffuse nuclear localization of wild-type GFP-DPF2 in human HEK293 cells, whereas pathogenic PHD variants form nuclear aggregates; FLAG and COS7 controls are separate experiments. Refine the broad nuclear claim to the independently supported nucleoplasm and chromatin pools. This is nonexclusive target-level resolution using HPA and human chromatin-recruitment evidence, not a claim that the original assay separately visualized both pools or that chromatin has a nucleus ancestry edge. Proposed replacements: nucleoplasm chromatin |
| GO:0005634 nucleus | IEA GO_REF:0000120 | MODIFY | Reason: The combined electronic row includes the nuclear UniProt location and a mouse sequence. The human UniProt nuclear location has direct literature evidence; the mouse location itself is annotated by similarity to human and is not an independent localization experiment. Refine the broad nuclear claim to the independently supported nucleoplasm and chromatin pools. This is nonexclusive target-level resolution using HPA and human chromatin-recruitment evidence, not a claim that the original assay separately visualized both pools or that chromatin has a nucleus ancestry edge. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: UniProtKB:Q61103 SOURCE WEAK OR INFERRED Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. ensembl:ENSMUSP00000120125 SOURCE WEAK OR INFERRED Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. UniProtKB-SubCell:SL-0191 SUPPORTS TRANSFER Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. Proposed replacements: nucleoplasm chromatin |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Reason: The current HPA record matches DPF2/Q92785 and reports supported nucleoplasm localization. Both inspected antibodies show this pool in human cell lines. The record also contains non-nuclear pools in other cells, so nucleoplasm is not exclusive and the antibody data do not distinguish natural products. Supporting Evidence: GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9825847 | ACCEPT | Reason: The inspected Reactome MITF-M/SWI-SNF association at the TYRP1 promoter event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9825847 GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9932836 | ACCEPT | Reason: The inspected Reactome binding of the DPF1/2/3 set to the SMARCC1-containing scaffold event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9932836 GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9933238 | ACCEPT | Reason: The inspected Reactome binding of the SS18-containing ATPase module to that scaffold event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9933238 GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9934021 | ACCEPT | Reason: The inspected Reactome formation of neuronal-progenitor BAF event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9934021 GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9934022 | ACCEPT | Reason: The inspected Reactome binding of the DPF2/PHF10 set to the scaffold event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9934022 GO_REF:0000052 |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9934024 | ACCEPT | Reason: The inspected Reactome binding of the SMARCA4/BCL11-containing ATPase module event contains an explicit positive path through component or candidate sets to DPF2 entity 9727509 (Q92785 residues 2–391), located in nucleoplasm. This is a curator-modeled localization corroborated by human HPA observations; it does not assign an alternative candidate or ATPase activity to DPF2. Traversal establishes the selected positive path, not an exhaustive reaction graph. Supporting Evidence: Reactome:R-HSA-9934024 GO_REF:0000052 |
| GO:0005737 cytoplasm | EXP PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | MODIFY | Reason: The source cytoplasmic assertion is retained as a real non-nuclear pool. Current HPA antibody records support cytosol and centrosome in U-251MG, cytosol in KOLF2.1J and vesicular staining in U-2 OS. The saved U-2 OS image places the annotated puncta within the cellular cytoplasm, supporting cytoplasmic vesicle rather than unrestricted vesicle. Vesicle identity rests on the HPA annotation; neither the image nor the broad export identifier establishes an endosome, lysosome or transport function. These are complementary pools from distinct human cell contexts, not exclusive localization or individual findings attributed to the older source assay. |
| GO:0005737 cytoplasm | IEA GO_REF:0000120 | MODIFY | Reason: The combined electronic source includes a human literature-supported cytoplasmic location. The mouse location is by similarity and is not counted as independent experimental grounding. Current HPA antibody records support cytosol and centrosome in U-251MG, cytosol in KOLF2.1J and vesicular staining in U-2 OS. The saved U-2 OS image places the annotated puncta within the cellular cytoplasm, supporting cytoplasmic vesicle rather than unrestricted vesicle. Vesicle identity rests on the HPA annotation; neither the image nor the broad export identifier establishes an endosome, lysosome or transport function. These are complementary pools from distinct human cell contexts, not exclusive localization or individual findings attributed to the older source assay. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: UniProtKB:Q61103 SOURCE WEAK OR INFERRED Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. ensembl:ENSMUSP00000120125 SOURCE WEAK OR INFERRED Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. UniProtKB-SubCell:SL-0086 SUPPORTS TRANSFER Human location has direct literature and HPA support; the mouse location is by similarity to human, so it is not independent experimental confirmation. Supporting Evidence: GO_REF:0000120 GO_REF:0000052 |
| GO:0005829 cytosol | IDA GO_REF:0000052 | KEEP AS NON CORE | Reason: The source and current HPA target record support a cytosolic pool, including antibody-level observations in U-251MG and KOLF2.1J cells. It is retained as non-core because the defined histone-reader and transcription-coregulator mechanisms are nuclear; this does not imply that cytosolic DPF2 is inactive or artifactual. Supporting Evidence: GO_REF:0000052 |
| GO:0006338 chromatin remodeling | NAS PMID:10078207 Reconstitution of a core chromatin remodeling complex from S... | ACCEPT | Reason: The historical study reconstitutes remodeling with BRG1/hBRM and conserved core subunits rather than demonstrating isolated DPF2 catalysis. Independent human DPF2 studies establish its histone-recognition, recruitment and SWI/SNF-associated regulatory contribution, which is participation in remodeling as an accessory subunit. Retain the process without giving DPF2 an ATPase molecular function. |
| GO:0006355 regulation of DNA-templated transcription | IBA GO_REF:0000033 | MODIFY | Reason: The literal PTN008700032 transcription-regulation IBD is ancestral to the authenticated DPF2 leaf and is grounded in experimental descendant records; donor number and the broad family are not treated as failures. Human DPF2 integrated-promoter and myeloid experiments resolve the supported activity to regulation of RNA polymerase II transcription. Refine specificity without rejecting the conserved regulatory inference. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: PANTHER:PTN008700032 · PTN008700032 SUPPORTS TRANSFER Literal IBD and target descent verified in PTHR45888; the target MSA sequence exactly matches the 391-residue canonical product. Proposed replacements: regulation of transcription by RNA polymerase II |
| GO:0006357 regulation of transcription by RNA polymerase II | NAS PMID:18809673 BRD7, a novel PBAF-specific SWI/SNF subunit, is required for... | MODIFY | Reason: The original source recovers tagged BAF45D in SWI/SNF complexes, including BRG1, ARID2 and ARID1A association; it is not treated as a DPF2-free study because BRD7 is foregrounded. Refine the broad regulatory term to both supported directions using independent target-specific experiments. In human cells, DPF2 associates with p52 and SWI/SNF components, is recruited with RelB/Brm to a lymphotoxin-responsive promoter, and enhances RelB/p52 activity in integrated reporters. These observations support a performed linking and coactivation role, beyond knockdown necessity alone. Separate human myeloid experiments connect DPF2 histone-pocket-dependent promoter recruitment with repression at differentiation-related loci. The signed refinements preserve activating and repressive contexts without assigning both experiments to the original complex-isolation source. |
| GO:0006915 apoptotic process | TAS PMID:8812431 The d4 gene family in the human genome. | KEEP AS NON CORE | Reason: The human d4-family paper places REQ/DPF2 in the family, while the foundational functional experiment is mouse Requiem antisense suppression in IL-3-dependent FDCP-1 cells. Preserve the curator assertion as a contextual apoptosis association supported by that ortholog evidence, not as a demonstrated universal human execution mechanism or a separate core activity. |
| GO:0016514 SWI/SNF complex | NAS PMID:8804307 Diversity and specialization of mammalian SWI/SNF complexes. | ACCEPT | Reason: SWI/SNF membership is corroborated by target-specific human DPF2 complex purification and endogenous association studies. The historical citation establishes the complex framework, while later evidence identifies DPF2 itself. The broad complex term accommodates the experimentally examined compositions without forcing all DPF2 into one cell-type-specific subtype. |
| GO:0030071 regulation of mitotic metaphase/anaphase transition | NAS PMID:25066234 Requirement for PBAF in transcriptional repression and repai... | UNDECIDED | Reason: The accessible full main paper directly examines PBAF-dependent transcriptional silencing and repair at DNA breaks; its discussion of sister-chromatid cohesion is not a direct DPF2 metaphase/anaphase-transition assay. The supplementary access attempt did not yield the document, and the particular DPF2 mechanism behind this historical NAS assertion remains unresolved. Preserve the source rather than infer a wrong-gene error or universal absence from the inspected scope. Supporting Evidence: |
| GO:0062072 histone H3K9me2/3 reader activity | IDA NOT PMID:29429572 Mutations in the BAF-Complex Subunit DPF2 Are Associated wit... | UNDECIDED | Reason: The imported NOT assertion is preserved, but its negative scope cannot be reconciled confidently with the source Results and Figure 3A: wild-type GST-DPF2 binds H3K9me2 and H3K9me3 peptides, whereas several pathogenic variants weaken those interactions. This prevents a simple absence claim. The source does not resolve how the measured methylated-tail interactions relate to the curated negative reader assertion or to a methylmark-dependent chromatin function. UNDECIDED records that conflict; it neither requires an affinity advantage for every reader term nor introduces a positive methylmark-reader annotation. Supporting Evidence: PMID:29429572 H3K14ac, H3K9ac, H3K9/14ac, H3K9me2, and H3K9me3 |
| GO:0070316 regulation of G0 to G1 transition | NAS PMID:11790558 SWI/SNF chromatin remodeling and cancer. | UNDECIDED | Reason: The accessible source is a review of SWI/SNF and cancer, without a recoverable DPF2-specific G0-to-G1 experiment. A general chromatin-regulatory role does not settle this particular transition. Retain the historical assertion unresolved, without interpreting abstract silence as contradictory evidence. Supporting Evidence: |
| GO:0097190 apoptotic signaling pathway | TAS PMID:7961935 Requiem: a novel zinc finger gene essential for apoptosis in... | KEEP AS NON CORE | Reason: The separately recovered original describes mouse FDCP-1 cells: antisense Requiem suppression permits survival after IL-3 withdrawal, with stable-transfection and conditioned-medium controls. This supports the retained context-dependent apoptosis annotation, but it does not identify an autonomous DPF2 signaling reaction or a human-product-specific execution mechanism. No additional process is proposed from necessity alone. Supporting Evidence: PMID:7961935 prevented the programmed cell death response following IL-3 deprivation by causing antisense suppression |
| GO:0140015 histone H3K14ac reader activity | IDA PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | ACCEPT | Reason: Retain H3K14ac recognition as a histone-reader subactivity: purified human DPF2 tandem PHD fingers bind this peptide, and intact histone pockets support cellular histone association and target-chromatin recruitment. The current term defines recognition of H3K14ac without requiring exclusivity or an affinity advantage over unmodified H3. Under the reported 2017 ITC conditions, H3 and H3K14ac bind at approximately 1.0 and 1.1 micromolar, respectively. SAHA-sensitive cellular association is corroborating acetylation-context evidence, not proof by itself that H3K14 is the responsible cellular mark. This retains the positive recognition evidence without claiming intrinsic acetyl preference or transferring MOZ-specific structural and cellular results to DPF2. |
| GO:0140046 histone H4K16ac reader activity | IDA PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | ACCEPT | Reason: Retain H4K16ac recognition as a histone-reader subactivity based on the direct human DPF2 peptide assay together with cellular histone-pocket-dependent association and chromatin recruitment. The current definition does not require an affinity advantage over unmodified H4: the reported values are approximately 30.2 micromolar for H4 and 50.4 micromolar for H4K16ac. SAHA-sensitive cellular association supports an acetylation context but does not identify H4K16 as its unique cause. No acetyl selectivity, equivalence to the stronger H3 interaction or autonomous remodeling catalysis is asserted. Supporting Evidence: |
| GO:1902459 positive regulation of stem cell population maintenance | NAS PMID:19279220 An embryonic stem cell chromatin remodeling complex, esBAF, ... | UNDECIDED | Reason: The available cache contains the mouse esBAF abstract and discussion but lacks the operative Results and Methods despite its full-text flag. The current esBAF definition includes DPF2, yet complex membership and Brg-dependent stem-cell maintenance do not resolve DPF2-specific positive regulation of stem-cell population maintenance. Bounded original-access attempts failed, so the source-specific process assertion remains undecided rather than being rejected. Supporting Evidence: |
| GO:1905454 negative regulation of myeloid progenitor cell differentiation | IBA GO_REF:0000033 | KEEP AS NON CORE | Reason: The target descends from PTN002578083, and the literal negative-myeloid-differentiation IBD is grounded in the human target itself. This is legitimate experimental grounding, not circular propagation. Human DPF2 recruitment and differentiation experiments support the regulatory sign, retained as a cell-context outcome of its transcriptional coregulator activity rather than a separate core function. Propagation Review Root cause: NO FAILURE NON CORE Sources checked: PANTHER:PTN002578083 · PTN002578083 SUPPORTS TRANSFER Literal IBD and target descent verified in PTHR45888; the target MSA sequence exactly matches the 391-residue canonical product. UniProtKB:Q92785 · DPF2 SUPPORTS TRANSFER The target is valid experimental grounding for the IBD; its appearance in WITH/FROM is not circular. |
| GO:1905454 negative regulation of myeloid progenitor cell differentiation | IMP PMID:28533407 Histone-binding of DPF2 mediates its repressive role in myel... | KEEP AS NON CORE | Reason: The human hematopoietic/myeloid experiments connect an intact DPF2 histone-binding pocket and target-chromatin recruitment to inhibition of differentiation. Preserve this positive, signed biological result as a context-specific consequence of the reader/coregulator mechanism, not a claim that every natural product inhibits every myeloid lineage. Supporting Evidence: |
| 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 | Reason: The accessible original abstract establishes Rb/HDAC/SWI-SNF repression complexes in G1 and S-phase regulation, but the full DPF2-specific evidence is unavailable. Nuclear coregulator function alone cannot establish this particular G1/S-transition annotation. Keep the imported NAS claim unresolved; do not equate another complex member performing the assay with proof that DPF2 cannot participate. Supporting Evidence: |
| GO:2000781 positive regulation of double-strand break repair | NAS PMID:25066234 Requirement for PBAF in transcriptional repression and repai... | UNDECIDED | Reason: The recovered main original supports PBAF-dependent repression near DNA breaks and efficient repair, using BRG1 and BAF180 perturbations and rescue. It does not resolve the particular DPF2 contribution in the inspected experiments, and the supplement was unavailable. Historical DPF2 association with SWI/SNF assemblies does not alone settle this target-specific repair role; retain uncertainty without a categorical exclusion. Supporting Evidence: |
| GO:2000819 regulation of nucleotide-excision repair | NAS PMID:12215535 The SWI/SNF chromatin-remodeling factor stimulates repair by... | UNDECIDED | Reason: The accessible abstract demonstrates stimulation of human excision-nuclease repair by SWI/SNF on damaged mononucleosomes. The unavailable full paper prevents verification of the DPF2 participant and mechanism for this particular NAS claim. Its chromatin-reader activity makes the context plausible but is not sufficient to turn a complex-level repair experiment into a resolved DPF2-specific process. Supporting Evidence: |
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Download this section (compressed HTML)Q: How do histone modification, salt conditions and nucleosome context determine DPF2 recognition, given the different acetyl-preference results and strong H3K14 crotonylation binding?
Q: Does the natural 207-residue Q92785-2 product retain stable partner associations or transcriptional functions despite deletion of much of the zinc-finger region?
Q: What is the precise scope of the imported NOT H3K9me2/me3-reader assertion, given wild-type peptide binding but unresolved selective reading in physiological chromatin?
Q: Which DPF2-specific experiments establish the older cell-cycle, stem-cell-maintenance and DNA-repair annotations, rather than complex-level effects?
Experiment: Compare sequence-verified full-length DPF2 and the natural 207-residue product in matched stability, localization, partner-association and chromatin-recruitment assays.
Hypothesis: The natural shorter product may retain partner association while differing in histone-dependent recruitment.
Experiment: Measure matched modified and unmodified peptide and nucleosome binding under the same salt conditions, with folded-pocket controls, to distinguish broad histone recognition from modification selectivity.
Hypothesis: Histone modification selectivity depends on the assayed molecular context and solution conditions.
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