Human-cell interaction, nuclear imaging, tethered reporter and BCL6 reporter experiments establish corepression and HDAC association. Selected Results and construct Methods were read; the truncated short form behaves differently from long BCOR.

The normal abstract describes Sp1-corepressor interactions and knockdown effects. It supports a repression context but does not resolve every construct or pairwise assay.

The normal abstract describes an ataxia-centered interaction screen. The GOA row supplies the BCOR–USP7 pair; the original supplementary pair has not been independently re-audited.

The normal abstract and selected canonical full-text Results, supplemented by earlier indexed primary sections, describe the BCOR assembly, partner associations, HSP70 recovery and complex H2A ubiquitination. Direct BCOR interaction with RING1 or RNF2 was not detected; PCGF1 can bridge their association. RNF2 is the catalytic subunit; BCOR is reviewed as a contributing component.

Normal abstract and selected publisher sections describe human OFCD phenotypes and Xenopus laterality/Pitx2c experiments. Species-specific evidence and clinical versus experimental observations are distinguished.

Selected human OFCD mesenchymal-cell Results and ChIP Methods support BCOR-dependent repression and restrained mineralization. Promoter ChIP does not resolve intrinsic DNA binding, and the antibody does not recognize the mutant protein.

Selected human PRC1-family purification and chromatin Results define distinct complexes. The compaction comparison focuses on PRC1.4, so it is not a BCOR-specific heterochromatin-formation assay.

The normal abstract describes human chromatin-protein affinity proteomics. The BCOR–KDM2B association is independently corroborated, but the exact supplementary screen entry was not re-audited.

Selected Methods/Results include mouse B-cell assays and human HEK293 nuclear imaging of endogenous BCOR, as well as mixed construct experiments. The source is not uniformly mouse-only.

The normal abstract and source context describe a proteome-scale binary interaction map. Three curated BCOR interactions preserve the tested Q6W2J9-4 isoform; the individual supplementary entries were not re-audited.

The normal abstract describes quantitative interaction proteomics in HeLa cells. Listed BCOR pairs are corroborated by other complex evidence; individual supplementary values were not re-audited.

Selected endogenous NT2-cell Results confirm BCOR–PCGF1 association and distinguish BCOR-containing PRC1 from other PCGF1 interaction networks. No supplemental-table-wide claim is made.

Selected Results support CBX8 association with the BCOR complex, including endogenous human germinal-center cells, and contextual cooperation with BCL6 and PRC2. Association can be mediated through RING1B.

The normal abstract reports a human Polycomb affinity-proteomics map. BCOR–PCGF1 and BCOR–CBX8 associations are corroborated by other papers, while the exact supplementary screen rows remain unaudited.

The normal abstract describes two human cell-background interaction networks. The original BCOR–PCGF1 pair and its cell assignment were not independently recovered; other primary evidence corroborates the association.

The normal abstract describes endogenous tagging, imaging and interaction proteomics. The exact BCOR–USP7 dataset entry was not re-audited.

Normal abstract and selected external Results identify mutation-dependent interaction screening, including AKT1 E17K. The BCOR-specific wild-type/mutant comparison remains unresolved.