Affinage

BCCIP

BRCA2 and CDKN1A-interacting protein · UniProt Q9P287

Length
314 aa
Mass
36.0 kDa
Annotated
2026-06-09
36 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BCCIP is a nuclear protein that integrates DNA double-strand break repair, cell-cycle checkpoint control, ribosome biogenesis, and mitotic fidelity, and exists as two alternatively spliced isoforms (BCCIPα/TOK-1α and BCCIPβ) sharing an internal conserved domain but differing in their C-termini (PMID:11313963, PMID:15713648). Through a shared region both isoforms bind the internal conserved region of BRCA2, and their depletion sharply reduces RAD51 and BRCA2 nuclear focus formation and homologous recombination repair of DSBs without affecting non-homologous end joining (PMID:11313963, PMID:15713648, PMID:17947333). BCCIPβ acts directly at the recombination step: it binds DNA and RAD51 and stimulates RAD51 homologous pairing by inducing a filament conformational change that promotes ADP release to maintain an active presynaptic filament (PMID:27694622). Beyond canonical break repair, BCCIP is recruited to stalled replication forks and protects nascent DNA from MRE11-mediated degradation (PMID:35592921). In cell-cycle control, the α isoform binds the C-terminus of p21 and cooperatively enhances p21-dependent inhibition of CDK2, while BCCIP is required for nuclear localization of p21, for p53 tetramerization, and for p53-dependent transactivation of p21 and HDM2, thereby enforcing the G1/S checkpoint after ionizing radiation (PMID:10878006, PMID:17135243, PMID:19713748). The two isoforms are also functionally specialized in other compartments: BCCIPβ serves as a nuclear chaperone for ribosomal protein RPL23/uL14 and, in the nucleolus, drives 12S pre-rRNA processing and 60S ribosome biogenesis through recruitment of eIF6 (PMID:25150171, PMID:33245766), whereas BCCIPα localizes to the mitotic spindle pole and centrosome and binds and inhibits FAM46/TENT5 poly(A) polymerases via an isoform-specific fold (PMID:28394342, PMID:37018411). BCCIP expression is set by an INO80/YY1-driven autoregulatory transcriptional circuit (PMID:27535137, PMID:29932276). In vivo, partial BCCIP loss produces genomic instability, chromosomal aberrations, and tumorigenesis, while complete loss is lethal to proliferative tissues and is not rescued by p53 deletion (PMID:21966279, PMID:24145349, PMID:33039352).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2000 High

    Established the first molecular partner of the α isoform, defining BCCIP as a CDK-inhibitory cofactor by showing it strengthens p21 action.

    Evidence Yeast two-hybrid cloning, ternary-complex co-IP, and in vitro CDK2 histone H1 kinase assay

    PMID:10878006

    Open questions at the time
    • Did not address the β isoform or DNA-repair roles
    • No structural basis for the p21 interaction
  2. 2001 Medium

    Identified BCCIPα as a BRCA2-interacting nuclear protein whose overexpression suppresses cancer cell growth, linking BCCIP to the BRCA2 axis and tumor suppression.

    Evidence Yeast two-hybrid, subcellular fractionation/immunofluorescence, growth inhibition assays

    PMID:11313963

    Open questions at the time
    • Functional consequence of the BRCA2 interaction not yet tested
    • Domain architecture defined but functions of NAD/ICD/CVD unassigned
  3. 2004 Medium

    Connected BCCIP to checkpoint control by showing it regulates p21 in a p53-dependent manner and that the β isoform delays G1/S progression.

    Evidence RNAi knockdown, p21-null rescue, flow cytometry, p53 reporter assay after ionizing radiation

    PMID:14726710 PMID:15539944

    Open questions at the time
    • Mechanism of p53 regulation unresolved at this stage
    • Did not separate checkpoint role from repair role
  4. 2005 High

    Demonstrated that both isoforms bind BRCA2 and are quantitatively required for RAD51/BRCA2 focus formation and HRR, placing BCCIP functionally in the homologous recombination pathway.

    Evidence Reciprocal co-IP, RNAi, immunofluorescence colocalization, HRR reporter assay

    PMID:15713648

    Open questions at the time
    • Whether BCCIP acts directly on RAD51 or via BRCA2 not yet distinguished
    • Step in HR affected unknown
  5. 2006 High

    Resolved the p53 regulatory mechanism by showing BCCIP is required for p53 tetramerization and promoter binding rather than p53 stabilization.

    Evidence RNAi, luciferase reporter, ChIP, native PAGE for tetramer assessment

    PMID:17135243

    Open questions at the time
    • How BCCIP promotes tetramer formation mechanistically unknown
    • Direct vs indirect p53 contact not established
  6. 2007 Medium

    Dissected BCCIP domains in HR and revealed that its loss drives genomic instability through spindle/centrosome defects and failed cytokinesis, broadening its role beyond repair.

    Evidence Domain-fragment overexpression with HR/NHEJ reporters and comet assay; RNAi with karyotyping, centrosome IF, and cytokinesis imaging

    PMID:17452982 PMID:17947333

    Open questions at the time
    • Molecular target at the spindle/centrosome unidentified
    • Link between repair defect and ploidy defect not mechanistically connected
  7. 2008 Medium

    Defined temporal dynamics of BCCIP at damage sites and identified upstream and signaling partners (LYRIC/AEG-1 degradation, PTPmu/Src phosphorylation).

    Evidence Immunofluorescence/FRAP at damage sites; co-IP, proteasome rescue, in vitro kinase/phosphatase assays, neurite outgrowth assay

    PMID:18413737 PMID:18440304 PMID:18773424

    Open questions at the time
    • Physiological significance of Src/PTPmu phosphorylation unclear
    • How AEG-1-driven degradation is regulated in vivo unknown
  8. 2009 Medium

    Showed BCCIP controls the subcellular distribution of p21, with a DNA-damage-enhanced interaction driving p21 nuclear retention independent of Thr-145 phosphorylation.

    Evidence FRET, subcellular fractionation, immunofluorescence, RNAi

    PMID:19713748

    Open questions at the time
    • Mechanism by which damage enhances the interaction unknown
    • Transport machinery involved not identified
  9. 2011 High

    Provided in vivo confirmation that BCCIP maintains chromosome stability and RAD51 function, and that its essentiality is p53-independent.

    Evidence Conditional knockdown mouse, sister chromatid union/break analysis, RAD51 IF, p53 knockout epistasis

    PMID:21966279

    Open questions at the time
    • Cause of p53-independent lethality not defined
    • Tissue specificity of phenotype not yet explored
  10. 2013 Medium

    Established BCCIP as a tumor suppressor whose transient loss initiates medulloblastoma but whose expression is required for tumor progression.

    Evidence Conditional knockdown mouse with p53 deletion, tumor histology, Shh pathway analysis, cassette-loss verification

    PMID:22292003 PMID:24145349

    Open questions at the time
    • Mechanism linking BCCIP loss to Shh alterations unknown
    • Why progression requires BCCIP re-expression not resolved
  11. 2014 Medium

    Identified an isoform-specific role for BCCIPβ as a nuclear chaperone for RPL23 acting with eIF6, first connecting BCCIP to ribosome biogenesis.

    Evidence Co-IP of ternary complex, fractionation, overexpression/depletion, immunofluorescence

    PMID:25150171

    Open questions at the time
    • Effect on mature ribosome output not measured here
    • Whether chaperone role contributes to genomic-instability phenotype unknown
  12. 2016 High

    Provided the mechanistic basis for BCCIP's HR function and revealed transcriptional control of the gene by INO80/YY1.

    Evidence Reconstituted in vitro DNA-binding, strand-exchange, ATPase, and filament conformation assays; siRNA, ChIP, reporter assays

    PMID:27535137 PMID:27694622

    Open questions at the time
    • How BCCIPβ recognizes the presynaptic filament structurally not determined
    • Integration of transcriptional control with damage signaling unknown
  13. 2017 Medium

    Localized BCCIPα to the mitotic spindle pole/centrosome, assigning a direct mitotic role to the α isoform.

    Evidence Confocal IF localization, RNAi, time-lapse mitotic imaging

    PMID:28394342

    Open questions at the time
    • Spindle-pole binding partner not identified
    • Mechanism of microtubule organization unresolved
  14. 2019 Medium

    Detailed the BCCIP-YY1 regulatory circuit, including an autoregulatory feedback loop and coordinate control of p53RE-mediated p21 transactivation.

    Evidence Co-IP, ChIP, reporter and ubiquitination assays, domain mapping, shRNA with rescue

    PMID:29932276 PMID:31035388

    Open questions at the time
    • How opposing YY1/BCCIP effects on p53RE are balanced unknown
    • In vivo relevance of the feedback loop not tested
  15. 2020 High

    Defined BCCIP's nucleolar role in 12S pre-rRNA processing and 60S biogenesis and showed that complete loss is catastrophic for proliferative stem/progenitor tissue.

    Evidence Fractionation/IF, pre-rRNA processing assay, eIF6 interaction mapping, conditional knockout MEFs and intestinal epithelium with organoids and RNA-Seq

    PMID:33039352 PMID:33245766

    Open questions at the time
    • Whether the ribosome defect underlies the lethality of complete loss not directly tested
    • Relationship between nucleolar and repair functions unresolved
  16. 2021 High

    Provided the first structure of BCCIPβ, revealing a GNAT-like fold with altered substrate/cofactor grooves and a conformationally dynamic flap implicated in partner binding.

    Evidence Two X-ray crystal structures of N-terminally truncated BCCIPβ

    PMID:33452718

    Open questions at the time
    • No demonstrated acetyltransferase activity despite GNAT similarity
    • Partner-bound structures not solved
  17. 2022 Medium

    Extended BCCIP's genome-protective role to replication stress by showing it shields nascent DNA from MRE11 nuclease at stalled forks.

    Evidence DNA fiber assay, MRE11 epistasis, γH2AX staining

    PMID:35592921

    Open questions at the time
    • Mechanism of fork recruitment not defined
    • Which isoform mediates fork protection unknown
  18. 2023 High

    Defined the structural basis for isoform divergence, showing BCCIPα adopts a unique fold that inhibits FAM46/TENT5 poly(A) polymerases, a function exclusive to the α isoform.

    Evidence Crystal structures of FAM46A/C–BCCIPα complexes, in vitro PAP assays, mutagenesis, isoform-specific binding

    PMID:37018411

    Open questions at the time
    • Cellular consequences of FAM46 inhibition by BCCIPα untested
    • How the α-specific function integrates with mitotic localization unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BCCIP's distinct activities — HR stimulation, replication-fork protection, p53/p21 checkpoint control, ribosome biogenesis, mitotic spindle organization, and FAM46 inhibition — are coordinated within a cell and which is rate-limiting for the essentiality and tumor-suppressor phenotypes remains unresolved.
  • No unified model reconciling the multiple compartment-specific functions
  • Biochemical activity of the GNAT-like fold undefined
  • Relative contribution of each function to lethality vs tumorigenesis unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140110 transcription regulator activity 2 GO:0003677 DNA binding 1 GO:0044183 protein folding chaperone 1
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 2 GO:0005730 nucleolus 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-73894 DNA Repair 3 R-HSA-8953854 Metabolism of RNA 2 R-HSA-69306 DNA Replication 1
Partners
BRCA2CDKN1AEIF6FAM46CRAD51RPL23TP53YY1

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 BCCIPα was identified as a novel nuclear protein that physically interacts with the internal conserved region of BRCA2 (encoded by exons 14-24). BCCIP is a nuclear protein with three distinct domains (NAD, ICD, CVD), and overexpression of BCCIPα inhibits breast and brain cancer cell growth. Yeast two-hybrid screen, nuclear localization by subcellular fractionation/immunofluorescence, cell growth inhibition assays Oncogene Medium 11313963
2000 TOK-1 (BCCIPα) was identified as a p21(Cip1) C-terminal-binding protein. TOK-1α, but not TOK-1β, directly binds the C-terminal proximal region of p21, forms a ternary complex with CDK2 via p21, and cooperatively enhances p21-dependent inhibitory activity toward CDK2 histone H1 kinase activity. Yeast two-hybrid cloning, co-immunoprecipitation (ternary complex), in vitro kinase assay (CDK2 histone H1 phosphorylation) The Journal of biological chemistry High 10878006
2005 Both BCCIPα and BCCIPβ isoforms interact with BRCA2 via a shared region. Chromatin-bound BRCA2 colocalizes with BCCIP nuclear foci. RNAi-mediated knockdown of BCCIPα (by 90%) or BCCIPβ (by 50%) markedly reduces RAD51 and BRCA2 nuclear foci and reduces homologous recombinational repair (HRR) of DSBs by 20- to 100-fold. Co-immunoprecipitation, RNA interference, immunofluorescence colocalization, HRR reporter assay Molecular and cellular biology High 15713648
2004 BCCIPβ binds p21 and inhibits cell growth; this growth inhibition is partially abrogated in p21-deficient cells. Overexpression of BCCIPβ delays G1-to-S progression and results in elevated p21 expression. Co-immunoprecipitation, p21-deficient cell rescue experiment, cell cycle analysis (flow cytometry), overexpression assay Cell cycle (Georgetown, Tex.) Medium 14726710
2004 BCCIP regulates p21 expression through a p53-dependent mechanism. RNAi-mediated partial knockdown of BCCIP reduces p21 levels and impairs G1/S checkpoint activation in response to ionizing radiation; BCCIP was shown to regulate p53 transcriptional activity. RNA interference, RT-PCR/western blot for p21 levels, G1/S checkpoint assay after ionizing radiation, p53-dependent transcription reporter assay Cell cycle (Georgetown, Tex.) Medium 15539944
2006 BCCIP is required for p53 transactivation activity. BCCIP knockdown by RNAi in p53 wild-type cells diminishes p53 transactivation without reducing p53 protein levels, inhibits p53 binding to the promoters of p21 and HDM2, and reduces tetrameric p53 formation. RNA interference, luciferase reporter assay, chromatin immunoprecipitation (ChIP), native PAGE for p53 tetramer assessment The Journal of biological chemistry High 17135243
2007 Multiple BCCIP domains independently regulate HR. BCCIP fragments interacting with BRCA2 or with p21 each inhibit DSB repair by HR. BCCIP does not affect non-homologous end joining (negative result). Constitutive BCCIP downregulation leads to increased spontaneous ssDNA and DSBs. Domain deletion/fragment overexpression, HR reporter assay, non-specific DNA integration assay (for NHEJ control), comet assay / ssDNA detection Nucleic acids research Medium 17947333
2007 BCCIP downregulation leads to chromosomal polyploidization, centrosome amplification, and abnormal mitotic spindle formation. BCCIP-knockdown cells enter mitosis and retain spindle checkpoint but fail to complete cytokinesis. RNAi knockdown, chromosome karyotyping, centrosome immunofluorescence, spindle checkpoint assay, live-cell imaging of cytokinesis Oncogene Medium 17452982
2008 RAD51 colocalizes with BCCIP early after ionizing radiation, and with RAD52 later. FRAP analysis shows BCCIP mobility does not change after hydroxyurea or ionizing radiation, whereas RAD52 mobility is reduced more by hydroxyurea. These data indicate temporally distinct RAD51-BCCIP and RAD51-RAD52 responses. Immunofluorescence colocalization, FRAP (fluorescence recovery after photobleaching) Cancer research Medium 18413737
2008 LYRIC/AEG-1 interacts with BCCIP and promotes proteasomal degradation of BCCIPα. Co-expression reduces BCCIPα protein levels, an effect partially abrogated by proteasome inhibition; a truncated LYRIC/AEG-1 lacking the interaction region did not alter BCCIPα levels. Yeast two-hybrid, co-immunoprecipitation, proteasome inhibitor rescue, truncation mutant analysis Biochemical and biophysical research communications Medium 18440304
2008 BCCIP interacts with receptor protein tyrosine phosphatase PTPmu. BCCIP is phosphorylated by Src tyrosine kinase and dephosphorylated by PTPmu in vitro. BCCIP is required for both permissive and repulsive functions of PTPmu in neurite outgrowth. Yeast two-hybrid, in vitro GST pulldown, in vitro kinase/phosphatase assay, neurite outgrowth assay with BCCIP knockdown Journal of cellular biochemistry Medium 18773424
2009 BCCIP is required for nuclear localization of p21. BCCIP downregulation reduces nuclear p21 and increases cytoplasmic p21. BCCIP-p21 interaction is enhanced in response to DNA damage (measured by FRET). This redistribution is not due to Thr-145 phosphorylation of p21. FRET (Fluorescence Resonance Energy Transfer), subcellular fractionation, immunofluorescence, RNAi knockdown, exogenous p21 expression Cell cycle (Georgetown, Tex.) Medium 19713748
2011 BCCIP deficiency in mouse embryonic fibroblasts causes a ~20-fold increase in sister chromatid union (SCU), 3.5-fold increase in chromatid breaks, reduced repair of irradiation-induced DNA damage, reduced RAD51 protein and nuclear foci, and impaired cell proliferation. p53 deletion cannot rescue embryonic lethality from BCCIP deficiency. Conditional knockdown transgenic mouse (Cre-LoxP RNAi), chromosome stability analysis, sister chromatid exchange assay, RAD51 immunofluorescence, p53 knockout epistasis PLoS genetics High 21966279
2012 BCCIP deficiency in the mouse neural system impairs embryonic and postnatal neural development, causing microcephaly and cerebellar defects associated with spontaneous DNA damage and cell death in proliferative neural progenitors. BCCIP deficiency impairs neural progenitor self-renewal and spontaneously activates p53. Conditional BCCIP knockdown mouse model (Cre-LoxP), neural spheroid culture, immunofluorescence for DNA damage markers, p53 activation assay PloS one Medium 22292003
2013 Conditional BCCIP knockdown combined with p53 deletion causes rapid medulloblastoma development with Sonic Hedgehog pathway alterations. Progressed tumors spontaneously lose the BCCIP knockdown cassette and restore BCCIP expression, demonstrating that transient BCCIP downregulation is sufficient to initiate tumorigenesis but BCCIP is required for tumor progression. Conditional knockdown transgenic mouse model, tumor histology, genomic analysis of Shh pathway, loss of knockdown cassette verification by PCR Cancer research Medium 24145349
2014 BCCIPβ, but not BCCIPα, forms a ternary complex with ribosomal protein RPL23/uL14 and pre-60S trans-acting factor eIF6 in a manner dependent on the intact C-terminal domain of BCCIPβ. BCCIPβ depletion reduces the free RPL23 pool and decreases nucleolar eIF6 levels. BCCIPβ overexpression leads to nucleoplasmic accumulation of extra-ribosomal RPL23, indicating BCCIPβ functions as a nuclear chaperone for RPL23. Co-immunoprecipitation, subcellular fractionation, overexpression/depletion experiments, immunofluorescence FEBS letters Medium 25150171
2016 BCCIPβ directly binds DNA and physically interacts with RAD51 to stimulate its homologous DNA pairing activity. BCCIPβ induces a conformational change within the RAD51 filament that promotes ADP release, thereby helping maintain an active presynaptic filament (stimulation is not due to filament stabilization). In vitro DNA binding assay, pulldown, in vitro D-loop/strand exchange assay, ATPase assay, filament conformational analysis Nucleic acids research High 27694622
2016 The INO80/YY1 chromatin remodeling complex transcriptionally regulates BCCIP expression. YY1 and INO80 are enriched at +0.17 kb downstream of the BCCIP transcriptional start site. Both INO80 and YY1 are required for recruiting the complex to the BCCIP promoter region; knockdown of either abolishes BCCIP mRNA and protein expression. siRNA knockdown, luciferase reporter assay, chromatin immunoprecipitation (ChIP), overexpression studies Protein & cell Medium 27535137
2017 BCCIPα localizes to the mitotic spindle pole and centrosome (proximal to the mother centriole). BCCIP depletion causes disoriented mitotic spindles, chromosome congression defects, and delayed mitotic progression, indicating BCCIP participates in microtubule organization. Immunofluorescence/confocal microscopy for spindle/centrosome localization, RNAi knockdown, time-lapse imaging of mitotic progression Oncogene Medium 28394342
2018 BCCIP directly interacts with YY1 via its ICD domain. BCCIP stabilizes YY1 by reducing YY1 ubiquitination, and YY1 in turn recruits itself to the BCCIP promoter to activate BCCIP transcription (BCCIP-YY1 autoregulatory feedback loop). BCCIP itself binds the BCCIP promoter in a YY1-dependent fashion. Co-immunoprecipitation, ChIP, luciferase reporter assay, ubiquitination assay, domain mapping with truncation constructs The FEBS journal Medium 29932276
2019 YY1 and BCCIP coordinately regulate p53-responsive element (p53RE)-mediated transactivation of p21. YY1, BCCIP, and p53 form cross-interacting complexes; YY1 inhibits while BCCIP enhances p53RE-mediated luciferase activity. BCCIP knockdown inhibits p53 and YY1 recruitment to the p53RE proximal region of p21 promoter. Co-immunoprecipitation, dual luciferase assay, ChIP, lentiviral shRNA knockdown, rescue by YY1 overexpression International journal of molecular sciences Medium 31035388
2020 A fraction of BCCIP localizes in the nucleolus and is required for a pre-rRNA processing step that produces 12S pre-rRNA (precursor to 5.8S rRNA) and for 60S ribosome biogenesis. Abrogation of BCCIP nucleolar localization or impaired BCCIP-eIF6 interaction compromises eIF6 recruitment to the nucleolus and 60S biogenesis. Subcellular fractionation and immunofluorescence for nucleolar localization, pre-rRNA processing assay (northern blot/PCR), eIF6 interaction mapping, conditional knockout MEFs Nucleic acids research High 33245766
2020 Complete deletion of Bccip in adult mouse intestinal epithelium causes rapid epithelial denudation (not rescued by Trp53 co-deletion), loss of proliferative capability of crypt progenitors, loss of crypt base columnar stem cell markers, and failure of crypt organoid growth in vitro. RNA-Seq showed overwhelming down-regulation of mitotic division genes. Conditional knockout mouse (Rosa26-CreERT2, Villin-CreERT2), crypt organoid culture, immunofluorescence, RNA-Seq The American journal of pathology Medium 33039352
2021 Crystal structures of N-terminal truncated human BCCIPβ (residues 61-314) show structural similarity to GCN5-related acetyltransferases (GNATs) but with altered acetyl-CoA and substrate-binding grooves. BCCIPβ contains a large 19-residue flap that adopts open or closed conformations and a positively charged, reduced substrate binding groove, suggesting binding sites for partner proteins. X-ray crystallography (two crystal structures solved) Protein science : a publication of the Protein Society High 33452718
2022 BCCIP is recruited to stalled replication forks and prevents MRE11 nuclease-mediated degradation of nascent DNA strands. BCCIP deficiency increases replication fork stalling and results in DNA double-strand break formation under replication stress. DNA fiber assay, iPOND (or proximity-ligation assay for fork recruitment), MRE11 inhibitor/knockdown epistasis, γH2AX staining FEBS letters Medium 35592921
2023 BCCIPα, but not BCCIPβ, binds FAM46 (TENT5) family noncanonical poly(A) polymerases and inhibits their PAP activity. Crystal structures of FAM46A/BCCIPα and FAM46C/BCCIPα complexes show BCCIPα adopts a unique fold (completely different from BCCIPβ) due to its distinct C-terminal segment; a helix-loop-helix segment in BCCIPα inserts into the active site cleft of FAM46 to inhibit PAP activity. The distinct C-terminal segment supports fold adoption but does not directly contact FAM46. X-ray crystallography (two complex structures), in vitro PAP activity assay, domain mutagenesis, isoform-specific binding assay Science advances High 37018411

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Inhibition of breast and brain cancer cell growth by BCCIPalpha, an evolutionarily conserved nuclear protein that interacts with BRCA2. Oncogene 81 11313963
2005 The BRCA2-interacting protein BCCIP functions in RAD51 and BRCA2 focus formation and homologous recombinational repair. Molecular and cellular biology 72 15713648
2000 TOK-1, a novel p21Cip1-binding protein that cooperatively enhances p21-dependent inhibitory activity toward CDK2 kinase. The Journal of biological chemistry 70 10878006
2008 LYRIC/AEG-1 overexpression modulates BCCIPalpha protein levels in prostate tumor cells. Biochemical and biophysical research communications 57 18440304
2008 Distinct RAD51 associations with RAD52 and BCCIP in response to DNA damage and replication stress. Cancer research 48 18413737
2003 Genomic structure of the human BCCIP gene and its expression in cancer. Gene 44 12527204
2007 BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage. Nucleic acids research 42 17947333
2007 Roles of BCCIP in chromosome stability and cytokinesis. Oncogene 41 17452982
2004 Inhibition of G1 to S cell cycle progression by BCCIP beta. Cell cycle (Georgetown, Tex.) 34 14726710
2006 Abrogation of the transactivation activity of p53 by BCCIP down-regulation. The Journal of biological chemistry 33 17135243
2004 BCCIP functions through p53 to regulate the expression of p21Waf1/Cip1. Cell cycle (Georgetown, Tex.) 31 15539944
2014 The beta-isoform of the BRCA2 and CDKN1A(p21)-interacting protein (BCCIP) stabilizes nuclear RPL23/uL14. FEBS letters 28 25150171
2013 BCCIP suppresses tumor initiation but is required for tumor progression. Cancer research 28 24145349
2017 Celecoxib enhances the radiosensitivity of HCT116 cells in a COX-2 independent manner by up-regulating BCCIP. American journal of translational research 24 28386336
2011 Essential roles of BCCIP in mouse embryonic development and structural stability of chromosomes. PLoS genetics 24 21966279
2009 BCCIP is required for the nuclear localization of the p21 protein. Cell cycle (Georgetown, Tex.) 24 19713748
2009 Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas. BMC cancer 23 19653894
2016 Human INO80/YY1 chromatin remodeling complex transcriptionally regulates the BRCA2- and CDKN1A-interacting protein (BCCIP) in cells. Protein & cell 22 27535137
2017 Regulation of spindle integrity and mitotic fidelity by BCCIP. Oncogene 21 28394342
2020 BCCIP is required for nucleolar recruitment of eIF6 and 12S pre-rRNA production during 60S ribosome biogenesis. Nucleic acids research 19 33245766
2016 The β-isoform of BCCIP promotes ADP release from the RAD51 presynaptic filament and enhances homologous DNA pairing. Nucleic acids research 19 27694622
2012 Requirement of mouse BCCIP for neural development and progenitor proliferation. PloS one 18 22292003
2023 Inhibition of FAM46/TENT5 activity by BCCIPα adopting a unique fold. Science advances 13 37018411
2007 Ortholog of BRCA2-interacting protein BCCIP controls morphogenetic responses during DNA replication stress in Ustilago maydis. DNA repair 12 17627904
2019 YY1/BCCIP Coordinately Regulates P53-Responsive Element (p53RE)-Mediated Transactivation of p21Waf1/Cip1. International journal of molecular sciences 10 31035388
2008 BCCIP associates with the receptor protein tyrosine phosphatase PTPmu. Journal of cellular biochemistry 10 18773424
2017 Roles of BCCIP deficiency in mammary tumorigenesis. Breast cancer research : BCR 8 29047390
2021 Structure of human BCCIP and implications for binding and modification of partner proteins. Protein science : a publication of the Protein Society 6 33452718
2019 The Penaeus stylirostris densovirus capsid protein interacts with the Litopenaeus vannamei BCCIP protein. Fish & shellfish immunology 6 30826413
2018 BCCIP binds to and activates its promoter in a YY1-dependent fashion in HCT116 cells. The FEBS journal 6 29932276
2016 High Expression of BCCIP β Can Promote Proliferation of Esophageal Squamous Cell Carcinoma. Digestive diseases and sciences 5 27995408
2013 Mutation analysis of the BCCIP gene for breast cancer susceptibility in breast/ovarian cancer families. Gynecologic oncology 4 23911796
2022 The BRCA2 and CDKN1A-interacting protein (BCCIP) stabilizes stalled replication forks and prevents degradation of nascent DNA. FEBS letters 3 35592921
2024 Expression and Significance of BCCIP and Glutathione Peroxidase 4 in Clear Cell Renal Cell Carcinoma. Bulletin of experimental biology and medicine 2 38342812
2020 Requirement of Bccip for the Regeneration of Intestinal Progenitors. The American journal of pathology 2 33039352
2025 Combined targeting of TCF7L1/2, PTEN, CDK6, and BCCIP by microRNA miR-29c-3p is associated with reduced invasion and proliferation of endometriotic cells. Reproductive medicine and biology 1 40135061

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