CTCF is a nuclear zinc-finger DNA-binding protein that organizes chromatin loops and regulates transcription. Sequence-specific occupancy at regulatory and boundary elements helps anchor contacts with cohesin and constrains enhancer–promoter communication. CTCF can activate or repress RNAPII transcription according to the locus and cellular context, and contributes to allele-specific organization at imprinted loci. RNA interactions can modulate its chromatin occupancy. CTCF also contributes to mitotic centromere organization. The 727-residue protein contains eleven zinc fingers; the 399-residue alternative product lacks the N-terminal 328 residues, and equivalent DNA recognition or architectural activity has not been established.
Definition: Binding to a protein that catalyzes histone demethylation.
Justification: CTCF associates with the histone demethylase KDM5B in DNase-treated cell extracts. GO:0019899 enzyme binding remains the supported available partner-class term. The captured immediate child list lacks a fitting histone-demethylase-binding child; a curator should check broader ontology coverage before creating this proposed class. The interaction does not establish demethylase activity or activation by CTCF, or purified binary contact.
Parent term: enzyme binding
Supporting Evidence:
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000122 negative regulation of transcription by RNA polymerase II | IDA PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | ACCEPT | Summary: The human MYC promoter experiments establish sequence-dependent repression. Reason: The human 293 cotransfections and mouse NIH3T3 stable reporters must be distinguished from the separate chicken-domain GAL4 assays in quail cells. Supporting Evidence: |
| GO:0000775 chromosome, centromeric region | IDA PMID:18550811 CTCF physically links cohesin to chromatin. | ACCEPT | Summary: Original metaphase immunofluorescence places CTCF at centromeric regions in primary human fibroblasts. Reason: This positive location does not itself establish regulation of sister cohesion. Supporting Evidence: |
| GO:0000775 chromosome, centromeric region | IDA PMID:26321640 CTCF Recruits Centromeric Protein CENP-E to the Pericentrome... | ACCEPT | Summary: CTCF occupies human centromeric and pericentromeric chromatin. Reason: Human HeLa ChIP detects CTCF at the selected satellite sites in G2/M, with target depletion reducing its occupancy. This is a direct chromosomal-location result, separate from the proposed consequences of recruiting CENP-E. It does not imply that all CTCF is centromeric. Supporting Evidence: |
| GO:0000775 chromosome, centromeric region | IEA GO_REF:0000044 | ACCEPT | Summary: The centromeric localization mapping is supported. Reason: The original UniProt subcellular-location mapping names SL-0047. Human centromeric staining and satellite-site ChIP independently support that compartment; no function is inferred from the location alone. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB-SubCell:SL-0047 SUPPORTS TRANSFER The literal UniProt location source is preserved and agrees with independently read target localization evidence; the mapping is not a new experiment. |
| GO:0000793 condensed chromosome | IDA PMID:16107875 CTCF binding and higher order chromatin structure of the H19... | ACCEPT | Summary: CTCF associates with condensed mitotic chromosomes. Reason: The externally recovered original reports HeLa and primary human amniocyte chromosome staining, biochemical fractionation and live GFP-construct localization. Fixation conditions affect detection, and the zinc-finger-containing region supports association. Separate mouse H19 experiments are not relabeled as human assays. Supporting Evidence: |
| GO:0000976 transcription cis-regulatory region binding | IDA PMID:18413740 DNA methyltransferase 1 and 3B activate BAG-1 expression via... | MODIFY | Summary: The BAG-1 promoter supports the RNAPII cis-regulatory binding refinement. Reason: The available original abstract, Introduction and Discussion explicitly describe CTCF binding at the BAG-1 upstream promoter and promoter deletion analysis. BAG-1 is a protein-coding RNAPII target, so GO:0000978 is more informative for this source than polymerase-unspecified cis-regulatory binding. The saved cache is marked full text but lacks its Methods and Results sections; this precision proposal combines those positive reports with established CTCF promoter binding and retains curator deference for the uninspected panels. Proposed replacements: RNA polymerase II cis-regulatory region sequence-specific DNA binding Supporting Evidence: PMID:18413740 preferential CTCF binding to the promoter region |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: Human CTCF directly recognizes regulatory MYC DNA. Reason: The actual 952-node current PTHR24404 tree places the target below the literal PTN002812688 IBD, with an exact donor-set join and no target-path loss record. The 727-residue alignment sequence is exact. The protected PTHR16515 cache and separate proposed PAINT variant are historical source contexts; neither their filenames nor target self-evidence indicate a phylogenetic defect. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002812688 SUPPORTS TRANSFER The exact IBD is on the verified 16-node target path in the current 952-node tree; its donor set matches the historical assertion and no target-path loss was found. Target self-evidence is legitimate. The old selected family cache is not silently replaced. Supporting Evidence: |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IDA PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | ACCEPT | Summary: The original human protein and defined finger fragments bind MYC regulatory DNA in sequence-discriminating assays. Reason: The downstream P2-proximal site is a cis-regulatory site; the original term and qualifier remain literal. Supporting Evidence: |
| GO:0000987 cis-regulatory region sequence-specific DNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: Conserved cis-regulatory sequence recognition is supported. Reason: The two source identifiers resolve to the same mouse Ctcf product, Q61164, rather than independent donors. Its current source records include experimental regulatory-DNA binding, and human CTCF motif-sensitive promoter assays independently agree. The broader electronic term is sound without claiming every mouse regulatory locus is conserved in human. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. Supporting Evidence: |
| GO:0001221 transcription coregulator binding | IPI PMID:31547883 CGGBP1 regulates CTCF occupancy at repeats. | UNDECIDED | Summary: The endogenous CTCF–CGGBP1 association is supported. Reason: The uncertainty is the specific partner class in GO:0001221: the source establishes a repeat-binding protein that regulates CTCF occupancy, but does not resolve whether the relevant interaction represents the non-DNA-binding coregulatory function described by that definition. DNA-binding capacity does not categorically preclude a separate coregulator role; a DNase-resistant complex also does not itself establish that role. Preserve the positive association and raise this class-scope question, rather than removing the interaction or automatically replacing it with DNA-binding transcription factor binding. Human fibroblast/HEK-293T endogenous reciprocal co-IP and PLA context; nuclear DNA-bridged and DNase-resistant fractions distinguished. No purified binary assay or exclusive short-product inference. Supporting Evidence: |
| GO:0001227 DNA-binding transcription repressor activity, RNA polymerase II-specific | IDA PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | ACCEPT | Summary: DNA binding joined to motif-sensitive human MYC reporter repression supports the specific RNAPII repressor activity, rather than a classification based solely on zinc fingers. Reason: DNA binding joined to motif-sensitive human MYC reporter repression supports the specific RNAPII repressor activity, rather than a classification based solely on zinc fingers. Supporting Evidence: |
| GO:0003677 DNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: The broad electronic DNA-binding assertion is correct. Reason: The exact mouse donor records include direct DNA-binding experiments, and human CTCF has sequence-discriminating binding activity established independently. Retain this conservative electronic assertion alongside the more informative sequence-specific annotations; it does not imply nonselective DNA binding or equal activity of the 399-residue product. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0003682 chromatin binding | IEA GO_REF:0000107 | ACCEPT | Summary: Chromatin binding is a conserved CTCF activity. Reason: Current mouse source records include chromatin-occupancy experiments; the UniProt and Ensembl identifiers are aliases for one Ctcf product. Human ChIP and mitotic chromatin association independently support the transfer. This annotation reports binding and does not by itself assert a particular remodeling enzyme activity. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0003700 DNA-binding transcription factor activity | IBA GO_REF:0000033 | MODIFY | Summary: The broad inherited transcription-factor premise is biologically sound. Reason: The inherited transcription-factor premise is biologically sound, with the exact PTN002812688 IBD on the verified target path and no target-specific loss. The human MYC and APP assays resolve the target activity as RNAPII-specific, motivating GO:0000981 without declaring the broader ancestor assertion false. The original donor set, including legitimate target evidence, is preserved. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Sources checked: PANTHER:PTN002812688 SUPPORTS TRANSFER The exact IBD is on the verified 16-node target path in the current 952-node tree; its donor set matches the historical assertion and no target-path loss was found. Target self-evidence is legitimate. The old selected family cache is not silently replaced. Proposed replacements: DNA-binding transcription factor activity, RNA polymerase II-specific |
| GO:0003700 DNA-binding transcription factor activity | IDA PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | MODIFY | Summary: The human MYC promoter work resolves the polymerase context. Reason: RNAPII-specific DNA-binding transcription-factor activity is a more informative target-level replacement for the broad original activity, with repression separately represented by its specific existing row. Proposed replacements: DNA-binding transcription factor activity, RNA polymerase II-specific Supporting Evidence: |
| GO:0003700 DNA-binding transcription factor activity | IDA PMID:9591631 A widely expressed transcription factor with multiple DNA se... | MODIFY | Summary: The reported MYC regulatory function supports a RNAPII transcription-factor refinement. Reason: The complete cached abstract explicitly describes CTCF binding to human MYC regulatory sequences and regulation of MYC transcription. GO:0000981 captures that protein-coding target context more precisely than polymerase-unspecified transcription-factor activity. Full access to this historical paper was not recovered, so exact construct details remain unverified; independent human MYC and APP transcription assays corroborate the biological class rather than replacing the original source identity. Proposed replacements: DNA-binding transcription factor activity, RNA polymerase II-specific Supporting Evidence: PMID:9591631 it can regulate its transcription in several experimental systems. |
| GO:0003723 RNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: The original mouse study directly demonstrates CTCF–Jpx RNA contact using UV-dependent RIP in female embryonic stem cells and purified-protein RNA pull-down and EMSA. Reason: The tested Jpx E1–E3 RNA gives dose-dependent binding with appropriate GFP/Xist controls. The current mouse IDA donor is real and the two WITH/FROM identifiers resolve to the same Ctcf product. Retain the conserved RNA-binding activity for human CTCF by ortholog transfer; this does not establish the same human JPX/XIST regulatory circuit, a loop-stabilizing mechanism, or activity of the 399-residue product. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:19505873 Complementary quantitative proteomics reveals that transcrip... | MODIFY | Summary: The cited source explicitly reports validated AP-4–CTCF interaction, and the official human TFAP4 record establishes the bHLH transcription-factor partner class. Reason: The current bHLH-binding term is more informative than protein binding. Its MRF child is not appropriate for TFAP4. This class refinement does not assign TFAP4 transcriptional activity to CTCF. The complete selected abstract explicitly names the interaction and AP-4 truncation validation. Full Methods/Results and exact truncation coordinates remain unavailable. Positive curated IPI and explicit abstract support are retained at this limited scope. Proposed replacements: bHLH transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:19536159 The pluripotency factor Oct4 interacts with Ctcf and also co... | MODIFY | Summary: OCT4/POU5F1 is an established sequence-specific transcription factor. Reason: The original has domain-mapped Ctcf–Oct4 binding and endogenous co-IP, supporting a partner-class refinement. It does not warrant transferring mouse X-chromosome-counting biology into a new human process annotation. The original main Results, Methods summary and binding figure distinguish mouse ES endogenous experiments, GST/S35 binding, and HEK-host transfection. The EMSA Oct4 construct is explicitly mouse; the supplementary Methods were not accessible, so not every fusion insert species/product is established by the accessible Methods summary. Proposed replacements: RNA polymerase II-specific DNA-binding transcription factor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:24725430 Vigilin interacts with CCCTC-binding factor (CTCF) and is in... | KEEP AS NON CORE | Summary: The current MINT record positively joins CTCF and RPL31 in a two-hybrid assay. Reason: RPL31 is a ribosomal protein, but binding the individual protein does not establish binding to an assembled RNA–protein complex or a role for CTCF in translation. No more specific class replacement is established. The abstract foregrounds vigilin and does not independently describe the RPL31 experiment; the curated target record supplies that positive pair. Exact fusion boundaries are unspecified and full paper Methods were not recovered here. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:24725430 Vigilin interacts with CCCTC-binding factor (CTCF) and is in... | KEEP AS NON CORE | Summary: Vigilin/HDLBP association is supported by the explicit primary abstract and four literal records spanning two-hybrid, reciprocal co-IP and pulldown. Reason: HDLBP RNA binding does not turn the partner into an assembled ribonucleoprotein complex or establish a specific adaptor activity for CTCF. The source metadata contain a discrepancy: raw host label is HEp-2/HeLa while the curator comment and abstract name HepG2/CNE1. A uniform cell-line assignment is unresolved. No full Methods or purified-binary claim. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:24937458 JARID1B is a luminal lineage-driving oncogene in breast canc... | MODIFY | Summary: KDM5B/JARID1B is an experimentally supported histone lysine demethylase. Reason: Positive source-specific co-IP supports binding to that enzyme class. The actual enzyme-binding child list and OLS comparison do not supply a fitting histone-demethylase-binding refinement; methyltransferase and deacetylase terms would be wrong. No CTCF demethylase activity is inferred. The experiments use DNase-treated nuclear extracts, human breast-cell panel, and Myc-His constructs. Six positive endogenous-cell records plus two tagged mutant records are not eight independent papers. SUM185PE absence and the K1435R reduced-interaction feature remain explicit; co-IP is not purified pairwise contact. Proposed replacements: enzyme binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | KEEP AS NON CORE | Summary: Three current IntAct records support the CTCF–ZMYM4 binary-screen interaction. Reason: Zinc fingers or a general DNA-binding annotation do not establish a sequence-specific transcription-factor or coregulator partner class. Preserve positive generic binding without manufacturing an activity. The curated source records report validated yeast two-hybrid screening. Selected cache is incomplete despite its full-text flag; a target-specific original table was not independently inspected. Record repetition represents assay/curation records, not three independent studies. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:26321640 CTCF Recruits Centromeric Protein CENP-E to the Pericentrome... | MODIFY | Summary: The source directly supports CTCF association with the kinesin CENP-E, including native co-IP and fragment mapping. Reason: Kinesin binding is more informative than generic protein binding and does not assign motor activity to CTCF. No fixed native complex stoichiometry is asserted. Human K562 extracts and purified bacterial MBP-CENPE fragments were compared with wheat-germ translated full-length human CTCF; both sides were not purified homogeneous proteins. The Results map residues 2528–2701, with narrower language in Discussion preserved rather than silently harmonized. CTCF N-terminal association and recruitment context supported. Proposed replacements: kinesin binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | KEEP AS NON CORE | Summary: Positive HuRI records identify ZMYM6 isoform4, not an unspecified full-length family protein. Reason: The official 170-aa reference sequence matches the ROGID, whereas assay features identify the sufficient 1–156 region. That evidence supports contextual binding without a demonstrated transcription-coregulator class or native interaction for every product. The source records use distinct GAL4 tags. Whole-backbone sequence identity does not erase the explicit assayed region or establish expression of the short product in native cells. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | MODIFY | Summary: The positive HuRI pair involves full-reference TRAF2, whose official evidence-backed record supports E3 ubiquitin-protein ligase activity. Reason: The E3-binding class is more informative than generic protein binding. This is not a claim that CTCF is ubiquitinated by TRAF2, activates its catalytic activity or participates in TNF signaling. The source records are positive GAL4-tagged two-hybrid observations with 727/501-residue reference backbones. No target-specific mammalian functional assay or direct ubiquitination result claimed. Proposed replacements: ubiquitin protein ligase binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | KEEP AS NON CORE | Summary: Retain the positive APP–CTCF screen association with its actual variant/assay boundaries. Reason: The raw records carry an APP mutation-disrupting-interaction feature at 670–671 while recording a positive interaction; their canonical 770-aa ROGID identifies the backbone, not an unmodified full-length test construct. No APP-receptor or amyloid-binding class replacement is established. The original main Results and general Methods were accessible, but the APP-specific supplementary table was not independently inspected. The paper uses full ORFs or fragments, but these three records specify mutation features, not deletion coordinates. The mutation feature does not establish an APP fragment interval, wild-type native receptor binding, or a negative interaction. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | KEEP AS NON CORE | Summary: The exact BioPlex record supports association of tagged RPL31 with CTCF in HCT116 cells. Reason: An affinity-isolation/MS association is retained without asserting purified pairwise contact or assembled-ribosome binding. The source records specify anti-tag affinity isolation and a C-terminal tandem tag on RPL31. Selected cache is partial despite full-text flag; the complete original Supplementary Table 1 was not independently inspected. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:35271311 OpenCell: Endogenous tagging for the cartography of human ce... | KEEP AS NON CORE | Summary: Retain the curated contextual RPL31 association with explicit deference: the same partner pair has independent positive literal two-hybrid and BioPlex records. Reason: This does not independently authenticate its OpenCell-specific measurement. An isolated ribosomal-protein partner does not justify ribonucleoprotein-complex binding or a translation function. The accessible original main text describes endogenous split-fluorescent tagging and triplicate IP-MS. Target Table S4 was not recovered; no current exact pair in selected IntAct/MINT. Paper-specific target-table verification remains unresolved. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:40205054 Multimodal cell maps as a foundation for structural and func... | KEEP AS NON CORE | Summary: Retain the curated contextual RPL31 association using the independently demonstrated pair as corroboration while keeping the 2025 source-specific target observation unverified. Reason: AP-MS membership/co-purification does not establish direct contact or binding to the complete ribosome. The accessible original Methods describe lentiviral HA-Flag U2OS baits, AP-MS, CompPASS/CompPASS-Plus filtering. Current raw pair join is empty and the target-specific supplementary/portal row was not inspected. The empty current join does not establish absence of the interaction. Positive generic interactions are retained under the standing CLINGEN_MENDELIAN campaign instruction; no stronger performed activity is inferred. Supporting Evidence: |
| GO:0005634 nucleus | IDA PMID:28319062 CTCF genetic alterations in endometrial carcinoma are pro-tu... | ACCEPT | Summary: Human CTCF is nuclear in the tested endometrial cell model. Reason: HA-tagged human wild-type CTCF and the three tested cancer-associated variants showed nuclear staining in Ishikawa cells. The immunostaining Methods and results support nucleus at the assay resolution, without establishing exclusive localization or activity of the current short splice product. Supporting Evidence: |
| GO:0005634 nucleus | IDA PMID:31547883 CGGBP1 regulates CTCF occupancy at repeats. | ACCEPT | Summary: Endogenous human CTCF has positive nuclear localization evidence. Reason: The original human fibroblast and HEK293T imaging and association study detects nuclear CTCF as well as context-dependent cytoplasmic signal. Retain the positive nuclear assertion without converting it into an exclusive compartment or assigning its approximately 50-kDa band to the current 399-residue product. Supporting Evidence: |
| GO:0005634 nucleus | IDA PMID:9407128 The zinc finger protein CTCF binds to the APBbeta domain of ... | ACCEPT | Summary: Endogenous CTCF was purified from HeLa nuclear extracts and identified by peptide sequence and terminal antibodies. Reason: Nuclear localization is directly supported; this experiment does not define activity of the official shorter product. Supporting Evidence: |
| GO:0005634 nucleus | IEA GO_REF:0000120 | ACCEPT | Summary: The combined electronic nuclear-location inference is supported. Reason: Current ARBA00026330 has three fully matched branches using official family/domain or FunFam predicates and the human taxonomic lineage. The mouse ortholog source also has experimental nuclear-location evidence. These are combined methods, not multiple independent human localization assays. Human imaging independently supports nucleus; the separately retrieved PANTHER tree version does not rewrite the rule predicates. Propagation Review Root cause: NO FAILURE CORE Sources checked: ARBA:ARBA00026330 SUPPORTS TRANSFER Current rule conditions were evaluated literally against official target xrefs and taxonomy. Positive branch matches authenticate rule application; the biological claim is assessed independently in the review reason. UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: The HPA experiment supports nucleoplasmic localization. Reason: The authentic HPA target record names P49711/CTCF and reports supported nucleoplasmic ICC/IF localization in A-431, U-251MG and U2OS cells. The source is gene-level antibody imaging, not evidence that both numbered products were separately detected. Supporting Evidence: GO_REF:0000052 |
| GO:0005654 nucleoplasm | IDA PMID:16107875 CTCF binding and higher order chromatin structure of the H19... | ACCEPT | Summary: Interphase nucleoplasmic CTCF is directly observed. Reason: The externally recovered source describes interphase nuclear distribution and chromosome-associated redistribution during mitosis in human cells. Nucleolar accumulation in some transfected clones is a separate context and does not invalidate positive nucleoplasmic localization. Supporting Evidence: |
| GO:0005654 nucleoplasm | IDA PMID:16595548 Targeting of CTCF to the nucleolus inhibits nucleolar transc... | ACCEPT | Summary: The reported nucleoplasm-to-nucleolus redistribution supports nucleoplasmic presence. Reason: The complete abstract explicitly reports CTCF movement from nucleoplasm to nucleolus after K562 differentiation or MCF7 apoptosis induction. Full original Methods were inaccessible, so this positive established localization is retained with curator deference rather than an invented detailed assay read. The rat neuronal observations are separate from the human cell experiments. Supporting Evidence: |
| GO:0005654 nucleoplasm | IEA GO_REF:0000044 | ACCEPT | Summary: The UniProt nucleoplasm mapping agrees with direct human evidence. Reason: The original SL-0190 mapping is preserved. HPA immunofluorescence and the independent human-cell localization papers support nucleoplasm without making it an exclusive cellular compartment. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB-SubCell:SL-0190 SUPPORTS TRANSFER The literal UniProt location source is preserved and agrees with independently read target localization evidence; the mapping is not a new experiment. |
| GO:0005654 nucleoplasm | TAS Reactome:R-HSA-9944419 | ACCEPT | Summary: The Reactome target entity is explicitly nucleoplasmic. Reason: The binding event R-HSA-9944419 reaches P49711 through its free CTCF input and through CTCF in the CHD8/(CHD7) output complex. The target entity spans residues 1–727 and both paths carry nucleoplasm. This is an event/entity provenance claim, not a new direct assay of CTCF catalytic remodeling or the 399-residue product. Supporting Evidence: Reactome:R-HSA-9944419 |
| GO:0005694 chromosome | EXP PMID:26321640 CTCF Recruits Centromeric Protein CENP-E to the Pericentrome... | MODIFY | Summary: The chromosome assertion can be refined to its measured centromeric compartment. Reason: The source resolves the CTCF-associated chromosomal regions as centromeric/pericentromeric satellite DNA through human-cell ChIP and sequence-specific binding experiments. GO:0000775 is the informative location for these experiments. The separate binding and CENP-E recruitment results do not make CTCF a motor or imply every chromosomal CTCF site is centromeric. This refinement converges on the existing GO:0000775 IDA annotation from PMID:26321640 (row 2); it increases source-specific precision without adding biological coverage. The original EXP and IDA assertions remain separate. Proposed replacements: chromosome, centromeric region Supporting Evidence: |
| GO:0005694 chromosome | IEA GO_REF:0000044 | ACCEPT | Summary: The broad chromosome mapping is biologically supported. Reason: The literal UniProt SL-0468 mapping is retained. Mitotic chromosome association and chromatin occupancy provide independent support for this conservative electronic compartment; more specific source-based locations are represented separately. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB-SubCell:SL-0468 SUPPORTS TRANSFER The literal UniProt location source is preserved and agrees with independently read target localization evidence; the mapping is not a new experiment. |
| GO:0005730 nucleolus | IDA PMID:16595548 Targeting of CTCF to the nucleolus inhibits nucleolar transc... | ACCEPT | Summary: Context-dependent nucleolar localization is positively reported. Reason: The complete abstract reports nucleolar CTCF in human K562 and MCF7 cell contexts and in rat trigeminal neurons. Full original Methods remain inaccessible, so the positive curated assertion is retained with that limit. Its 180-kDa poly(ADP-ribosyl)ated form is a modification-defined form, not a demonstrated numbered splice isoform. Supporting Evidence: |
| GO:0006357 regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: The ancestral RNAPII regulatory assertion is supported. Reason: The actual current family tree places the target beneath the literal PTN002812688 IBD for this process, with the original donor set preserved and no target-path loss record found. Human promoter and locus experiments establish both positive and negative RNAPII regulation. Target self-evidence is legitimate descendant grounding, not circularity; the protected older family cache remains a separate source snapshot. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002812688 SUPPORTS TRANSFER The exact IBD is on the verified 16-node target path in the current 952-node tree; its donor set matches the historical assertion and no target-path loss was found. Target self-evidence is legitimate. The old selected family cache is not silently replaced. |
| GO:0008270 zinc ion binding | TAS PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | ACCEPT | Summary: The metal-dependent zinc-finger DNA-binding architecture is integral to the demonstrated activity. Reason: Finger deletion and zinc-dependent binding conditions support the retained structural metal-binding annotation; no soluble zinc-homeostasis role is inferred. |
| GO:0008285 negative regulation of cell population proliferation | IMP PMID:28319062 CTCF genetic alterations in endometrial carcinoma are pro-tu... | KEEP AS NON CORE | Summary: CTCF can inhibit proliferation in the tested tumor-cell context. Reason: In human endometrial cells, wild-type expression reduced the MTT proliferation endpoint and colony formation, whereas R377H/P378L lost those effects. The paper also reports no significant proliferation change after partial CTCF depletion in KLE cells, and colony formation can fall after either overexpression or depletion. Retain the contextual regulatory result without promoting universal growth suppression to a separate core activity. Supporting Evidence: PMID:28319062 Both R377H and P378L abrogated the growth inhibitory effects |
| GO:0010628 positive regulation of gene expression | IEA GO_REF:0000107 | ACCEPT | Summary: Positive gene-expression regulation is a valid conserved role. Reason: The literal mouse donor chain includes an experimental positive regulatory annotation as well as propagated records, and the two source identifiers identify one mouse gene product. Independent human MHC-II and APP experiments show positive transcriptional effects. The broad electronic process is retained without treating every donor record as an independent experiment. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0010628 positive regulation of gene expression | IMP PMID:18347100 The insulator factor CTCF controls MHC class II gene express... | MODIFY | Summary: The measured MHC-II response supports positive RNAPII transcriptional regulation. Reason: CTCF depletion in human Raji cells reduces HLA-DRB1/DQA1 transcripts and surface expression without reducing CIITA/RFX5 expression or globally suppressing RNAPII activity. The accompanying promoter contacts and chromatin-mark changes support an architectural contribution to these protein-coding loci. GO:0045944 is more precise than undifferentiated gene-expression regulation; the evidence does not assign CTCF an intrinsic histone-modifying activity. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: PMID:18347100 diminish expression of these genes |
| GO:0010629 negative regulation of gene expression | IEA GO_REF:0000107 | ACCEPT | Summary: Negative gene-expression regulation is a valid conserved role. Reason: Mouse Ctcf has a current experimental negative-regulation donor record, and human MYC and BAG-1 experiments independently support repressive contexts. The UniProt/Ensembl identifiers are aliases rather than independent support. Positive effects at other loci do not contradict this contextual negative function. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0040029 epigenetic regulation of gene expression | IEA GO_REF:0000117 | ACCEPT | Summary: The electronic epigenetic-regulation annotation is biologically sound. Reason: ARBA00033485 branch 52 matches the actual two FunFam predicates and human Hominidae lineage. Separately, original imprinting-control-region experiments connect CTCF site occupancy to inherited allele-specific looping and chromatin/methylation states. The rule match authenticates its application; the biological assessment comes from the primary evidence, without an intrinsic methyltransferase inference. Propagation Review Root cause: NO FAILURE CORE Sources checked: ARBA:ARBA00033485 SUPPORTS TRANSFER Current rule conditions were evaluated literally against official target xrefs and taxonomy. Positive branch matches authenticate rule application; the biological claim is assessed independently in the review reason. Supporting Evidence: |
| GO:0040029 epigenetic regulation of gene expression | IMP PMID:16815976 CTCF binding at the H19 imprinting control region mediates m... | ACCEPT | Summary: CTCF contributes directly to allele-specific epigenetic architecture. Reason: Neonatal mouse liver 3C and ChIP, parental-allele resolution and mutation of H19 imprinting-control-region CTCF sites connect CTCF occupancy to the maternal configuration restricting Igf2 enhancer access. The separate translated human protein experiments address binding, not an all-human imprinting model. Maintenance/propagation of the imprinted architecture is supported without claiming that CTCF establishes every germline methylation mark. Supporting Evidence: PMID:16815976 restrict enhancer access to Igf2 |
| GO:0043035 chromatin insulator sequence binding | IDA PMID:17827499 Critical DNA binding interactions of the insulator protein C... | ACCEPT | Summary: Purified human CTCF finger constructs bind the defined chicken beta-globin insulator FII and mouse H19/Igf2 regulatory sites. Reason: These are genuine insulator DNA substrates, without claiming that the assay used a complete human chromosomal insulator. Supporting Evidence: PMID:17827499 a core 12-bp DNA sequence common to most CTCF sites |
| GO:0043565 sequence-specific DNA binding | IDA PMID:17827499 Critical DNA binding interactions of the insulator protein C... | ACCEPT | Summary: Purified human CTCF fragments discriminate cognate sequences and base substitutions. Reason: This directly supports sequence-specific DNA binding across the tested sites; engineered fragments are not official isoform 2. Supporting Evidence: |
| GO:0043565 sequence-specific DNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: The ortholog-transfer sequence-specific DNA-binding term is supported. Reason: The current mouse donor records include direct sequence-binding annotations; human zinc-finger and motif-mutant assays independently agree. Retain the conservative electronic term without converting the selected cache family name into a phylogenetic judgment or treating the two mouse aliases as separate donors. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0045892 negative regulation of DNA-templated transcription | IDA PMID:18413740 DNA methyltransferase 1 and 3B activate BAG-1 expression via... | MODIFY | Summary: The BAG-1 repression context supports the RNAPII-specific process. Reason: The available original text explicitly reports CTCF promoter occupancy and inhibition of BAG-1 promoter activity in transient cotransfections, contrasting the positive BORIS context. GO:0000122 is the more precise process for this protein-coding promoter. The complete Methods/Results panels were not available in the selected extraction; preserve the experimental source and positive result with that access limit. Proposed replacements: negative regulation of transcription by RNA polymerase II Supporting Evidence: |
| GO:0045892 negative regulation of DNA-templated transcription | IDA PMID:8649389 An exceptionally conserved transcriptional repressor, CTCF, ... | MODIFY | Summary: The human MYC assay supports RNAPII-specific repression. Reason: The original source assessed in the bounded core consultation establishes sequence-dependent repression of the human MYC promoter. Refine the broader transcriptional process to GO:0000122. Its human protein/promoter experiments remain distinct from chicken terminal-domain GAL4 assays in quail cells; those are not silently relabeled as human CTCF product experiments. Proposed replacements: negative regulation of transcription by RNA polymerase II Supporting Evidence: |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:9407128 The zinc finger protein CTCF binds to the APBbeta domain of ... | MODIFY | Summary: The APP promoter competition assay in HeLa nuclear extract supports positive transcriptional regulation in a RNAPII promoter context. Reason: Refine that known specificity while preserving the source assertion; the experiment is not purified CTCF alone reconstituting transcription. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: PMID:9407128 CTCF acts as a transcriptional activator |
| GO:0045893 positive regulation of DNA-templated transcription | IMP PMID:19322193 Architectural roles of multiple chromatin insulators at the ... | MODIFY | Summary: Positive APOC3 transcription is a RNAPII-specific regulatory context. Reason: The actual human Hep3B/HeLa original links CTCF-site occupancy and CTCF depletion to APOC3 expression, promoter RNAPII/HNF4 recruitment and loop organization. GO:0045944 specifies this protein-coding transcriptional response. APOA1 responds in the opposite direction in the same locus, so the source supports contextual activation rather than a universal activator label. Proposed replacements: positive regulation of transcription by RNA polymerase II Supporting Evidence: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:24662484 Human colorectal cancer-specific CCAT1-L lncRNA regulates lo... | ACCEPT | Summary: CTCF occupancy at the MYC regulatory contacts and CTCF depletion with reduced MYC/CCAT1-L expression support positive RNAPII regulation in human colorectal cells. Reason: The CCAT1-L ASO-sequence corrigendum is acknowledged and does not withdraw these findings. Supporting Evidence: |
| GO:0070602 regulation of centromeric sister chromatid cohesion | NAS PMID:18550811 CTCF physically links cohesin to chromatin. | UNDECIDED | Summary: The original NAS source demonstrates centromeric localization and cohesin recruitment but explicitly leaves the precise mitotic consequence for later experiments. Reason: The newer human HCT116-AID study demonstrates centromere tension/plate maintenance; its partial-RAD21 comparator explicitly preserves sister cohesion. These positive results do not yet resolve this specific cohesion-regulation assertion. This is neither a wrong-gene claim nor a denial of mitotic function. |
| GO:0071459 protein localization to chromosome, centromeric region | IMP PMID:26321640 CTCF Recruits Centromeric Protein CENP-E to the Pericentrome... | KEEP AS NON CORE | Summary: CTCF-dependent centromeric recruitment of CENP-E is a supported mitotic context. Reason: In the 2015 human HeLa experiments, CTCF depletion reduced CENP-E occupancy at centromeric/pericentromeric sites, while CENP-E depletion did not comparably remove CTCF. A binding-competent CENP-E fragment also perturbed congression. These results support the localization process without assigning CTCF motor activity. The newer three-day HCT116 CTCF-AID study reports unchanged CENP-E recruitment, so the earlier result is retained at its specific cell/perturbation context rather than universalized. |
| GO:0071514 genomic imprinting | IDA PMID:17827499 Critical DNA binding interactions of the insulator protein C... | ACCEPT | Summary: Human CTCF performs methylation-sensitive binding to the mouse H19/Igf2 imprinting-control DNA, a concrete allele-discriminating step. Reason: Retain the original curated process assignment with this restricted biochemical scope; the paper does not measure human germline establishment, write DNA methylation, or demonstrate every stage of imprinting. Supporting Evidence: |
| GO:0140587 chromatin loop anchoring activity | IEA GO_REF:0000107 | ACCEPT | Summary: Retain the loop-anchoring activity. Reason: Human site-dependent cohesin recruitment and CTCF-bound contacts, together with directional binding-site perturbations, support architectural participation. The actual mouse Q61164 donor records include direct loop-anchor annotations; its Ensembl identifier is an alias for the same product. Retain the conserved activity without assigning the SMC extrusion motor, a fixed native stoichiometry, or equal function to the 399-residue product. The later mouse Jpx study supplies an additional direct donor experiment; RNA-sensitive anchor occupancy and motif-dependent contacts are distinguished from an unmeasured intrinsic extrusion or oligomerization mechanism. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:0140588 chromatin looping | IDA PMID:18654629 The insulator binding protein CTCF positions 20 nucleosomes ... | ACCEPT | Summary: Chromatin looping is biologically supported by independent human CTCF perturbation and contact measurements. Reason: Chromatin looping is supported by independent human CTCF perturbation and contact measurements. The preserved PMID:18654629 source studies nucleosome organization and discusses long-range contacts as prior work, rather than performing a loop assay. Its source-specific citation mismatch is recorded separately; PMID:24662484 supplies direct supporting evidence without changing the historical source identity. Supporting Evidence: |
| GO:0140588 chromatin looping | IDA PMID:24662484 Human colorectal cancer-specific CCAT1-L lncRNA regulates lo... | ACCEPT | Summary: The original human colorectal-cell ChIP and 3C experiments directly connect CTCF-bound sites to the measured MYC looping contacts. Reason: CTCF depletion reduces those contacts. The inferred RNA allostery/local concentration model is distinct from the measured result. Supporting Evidence: |
| GO:0140588 chromatin looping | IEA GO_REF:0000107 | ACCEPT | Summary: Retain the conserved looping biology, independently supported in human cells. Reason: The actual mouse donor has experimental looping records, and human CTCF-bound contact assays and binding-site inversions independently support conserved looping participation. CTCF supplies an architectural DNA-binding/anchoring contribution rather than the intrinsic extrusion motor. Q61164 and the Ensembl identifier are aliases for the same donor, not independent experiments. The later mouse Jpx study supplies an additional direct donor experiment; RNA-sensitive anchor occupancy and motif-dependent contacts are distinguished from an unmeasured intrinsic extrusion or oligomerization mechanism. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:1990837 sequence-specific double-stranded DNA binding | IEA GO_REF:0000107 | ACCEPT | Summary: Conserved sequence-specific double-stranded DNA recognition is supported. Reason: The current mouse donor has direct annotations from motif/anchor experiments. Independently read human-cell CRISPR inversion and in-vitro EMSA studies show sequence- and orientation-sensitive CTCF recognition of double-stranded binding sites. The protein in the EMSA is described as in-vitro synthesized without a numbered human product assignment; the 399-residue product is not assumed equivalent. The later mouse Jpx study supplies an additional direct donor experiment; RNA-sensitive anchor occupancy and motif-dependent contacts are distinguished from an unmeasured intrinsic extrusion or oligomerization mechanism. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. |
| GO:1990841 promoter-specific chromatin binding | IEA GO_REF:0000107 | ACCEPT | Summary: The original study detects endogenous CTCF at the mouse Xist promoter by ChIP, with differentiation- and allele-dependent occupancy. Reason: Purified CTCF binds P2 and upstream DNA in motif-dependent EMSA, while promoter mutation and reporter assays support a direct regulatory role. The current mouse IDA donor supports promoter-specific chromatin binding, a conserved CTCF capability. P1 ChIP without P1 EMSA binding does not establish direct P1 sequence recognition; the proposed P2-to-P1 loop is a hypothesis. Retain the human ortholog transfer without claiming a demonstrated human XIST mechanism. Propagation Review Root cause: NO FAILURE CORE Sources checked: UniProtKB:Q61164 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. ensembl:ENSMUSP00000005841 SUPPORTS TRANSFER Exact official identity resolves to mouse Ctcf; these UniProt and Ensembl identifiers are aliases for one product. Complete donor records and exact-term source joins are preserved, including experimental versus propagated methods. Source-specific biological limits are stated in the review reason. Supporting Evidence: |
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Download this section (compressed HTML)Q: Which CTCF activity directly modulates centromeric sister cohesion, as distinct from centromere spring structure and chromosome segregation?
Q: Which DNA-binding and chromatin-organization activities are retained by the official 399-aa product?
Q: Can the source citation for the original PMID18654629 looping row be updated to a direct loop study while preserving its historical identity?
Q: Does the CTCF–CGGBP1 interaction represent a separable non-DNA-binding coregulator role, or should its positive association receive a different partner-class term?
Q: How do cell type, depletion duration and mitotic state explain the distinct CENP-E recruitment outcomes in the 2015 and 2026 studies?
Q: How do the protected PTHR16515/PTHR16515:SF49 records and the current PTHR24404 target tree correspond across PANTHER resource versions? The target and its three on-path IBDs are authenticated in the latter; this version difference alone does not justify changing the selected family or rejecting the transfers.
Experiment: Compare the two sequence-verified human CTCF products at matched expression using motif-resolved DNA binding, chromatin occupancy and contact assays; distinguish engineered finger fragments from the natural short product.
Experiment: Use acute, matched CTCF perturbations in the original HeLa and HCT116 contexts to separate CENP-E recruitment, centromere tension, sister cohesion and chromosome congression endpoints.
The authorized normal fetch succeeded. The genuine Falcon research attempt timed out at its configured 90-second limit; the configured perplexity-lite fallback then returned HTTP 401 (insufficient quota). No successful provider report was produced. The preserved process and stdout/stderr receipts record both outcomes; no blind retry was made.
Subsequent evidence assessment is manual and source-specific. This file records the failed provider boundary and will identify actual manually consulted sources as research proceeds. It is not a provider-generated report.
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