Affinage

BARD1

BRCA1-associated RING domain protein 1 · UniProt Q99728

Length
777 aa
Mass
86.6 kDa
Annotated
2026-04-28
100 papers in source corpus 55 papers cited in narrative 55 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BARD1 is the obligate heterodimerization partner of BRCA1, forming a RING-type E3 ubiquitin ligase that is essential for genome maintenance through homology-directed DNA repair, replication fork protection, and transcription-coupled RNA processing. The BRCA1-BARD1 heterodimer, whose structure has been resolved by NMR and cryo-EM, ubiquitinates nucleosomal H2A at K125/K127/K129 and RNA polymerase II, assembles K6-linked and other non-K48 polyubiquitin chains, and directly stimulates RAD51-mediated synaptic complex formation and long-range DNA end resection by EXO1, DNA2-BLM, and DNA2-WRN (PMID:11278247, PMID:33589814, PMID:28976962, PMID:39261728). BARD1 provides multivalent chromatin recognition—its ankyrin repeat domain reads H4K20me0 on post-replicative chromatin and its BRCT-associated BUDR motif reads RNF168-generated H2AK15ub—to target the complex specifically to DNA double-strand breaks in S/G2, where it repositions 53BP1 via SMARCAD1 and recruits PALB2-RAD51; its BRCT domain independently recruits the complex to stalled replication forks via poly(ADP-ribose) binding, a function genetically separable from HDR (PMID:30804502, PMID:34321663, PMID:27239795, PMID:30244837). BARD1 also inhibits mRNA 3′-end processing through interaction with CstF-50 and directs ubiquitin-mediated degradation of stalled RNA polymerase II, and can promote apoptosis through BRCA1-independent mitochondrial translocation and Bax oligomerization (PMID:10477523, PMID:15905410, PMID:17510055).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1997 High

    Establishing that BARD1 is a nuclear, S-phase-regulated partner of BRCA1 resolved when and where the two proteins act together in the cell cycle.

    Evidence Immunofluorescence and cell fractionation across synchronized cell cycle stages

    PMID:9342365

    Open questions at the time
    • Mechanism of cell-cycle-dependent aggregation into nuclear dots unknown
    • No functional assay linked to co-localization
  2. 1999 High

    Discovery that BARD1 interacts with CstF-50 and inhibits mRNA polyadenylation established an unexpected connection between a DNA-repair-associated protein and RNA processing.

    Evidence In vitro binding assays, co-immunoprecipitation, and in vitro polyadenylation inhibition

    PMID:10477523

    Open questions at the time
    • Physiological substrates whose polyadenylation is regulated in vivo not identified
    • Mechanism by which BARD1-CstF interaction inhibits cleavage unclear
  3. 2001 High

    Demonstrating that the BRCA1-BARD1 RING heterodimer functions as an E3 ubiquitin ligase—and that cancer mutation C61G abolishes this—established the enzymatic activity central to almost all subsequent mechanistic work.

    Evidence In vitro ubiquitin ligase assays with purified RING domains; NMR solution structure of heterodimer; mutagenesis

    PMID:11278247 PMID:11573085

    Open questions at the time
    • Physiological substrates not yet identified
    • Ubiquitin chain linkage specificity not determined
  4. 2001 High

    BARD1 was shown to promote apoptosis independently of BRCA1, involving p53 stabilization, revealing a tumor-suppressive function beyond DNA repair.

    Evidence Overexpression and antisense repression of BARD1; co-IP with p53; apoptosis assays; Q564H disease mutation analysis

    PMID:11257228 PMID:11779501

    Open questions at the time
    • Direct mechanism of p53 stabilization unclear
    • In vivo relevance of BRCA1-independent apoptosis not demonstrated genetically
  5. 2002 High

    Identification of H2A/H2AX as substrates and non-K48 (including K6 and K63) polyubiquitin chains as products defined the signaling rather than degradative nature of BRCA1-BARD1 ubiquitination, while BARD1 was shown to control BRCA1 nuclear localization.

    Evidence In vitro ubiquitylation with lysine-specific ubiquitin mutants; nuclear fractionation and fluorescence microscopy with BARD1/BRCA1 mutants

    PMID:11925436 PMID:11927591

    Open questions at the time
    • K6-chain reader proteins unknown
    • Whether nuclear retention is the sole mechanism of BARD1-dependent BRCA1 function unclear
  6. 2003 High

    Bard1-null mouse embryonic lethality phenocopying Brca1 loss, and dominant-negative BARD1 peptides impairing HDR, genetically established that BRCA1 and BARD1 function as an obligate heterodimer for development and homologous recombination.

    Evidence Bard1 knockout mice with p53 epistasis; I-SceI HDR assay with dominant-negative BARD1 truncations

    PMID:12832489 PMID:14560035

    Open questions at the time
    • Which specific BARD1 domains are essential for HDR not mapped
    • Whether E3 activity is required for embryonic survival not tested
  7. 2004 High

    Demonstration that BRCA1-BARD1 catalyzes K6-linked ubiquitin conjugates at replication and DSB sites in vivo, and identification of NPM1 as a non-degradative substrate, expanded the functional substrate repertoire.

    Evidence K6 ubiquitin mutant expression; siRNA depletion; mass spectrometry substrate identification; in vitro and in vivo ubiquitylation

    PMID:14976165 PMID:15184379

    Open questions at the time
    • Functional consequence of NPM1 ubiquitination unclear
    • K6-chain specific antibodies/readers not available
  8. 2005 High

    BRCA1-BARD1 was shown to ubiquitinate elongating RNA Pol II (Ser5-phospho Rpb1), coupling its E3 activity to transcription-coupled damage responses and explaining the polyadenylation inhibition phenotype.

    Evidence In vitro ubiquitylation of Rpb1; siRNA knockdown stabilizing RNAP II after damage; in vitro 3′ cleavage assay

    PMID:15886201 PMID:15905410

    Open questions at the time
    • Whether RNAP II ubiquitination and polyadenylation inhibition are mechanistically linked or independent not resolved
    • In vivo transcriptome-wide consequences not assessed
  9. 2006 High

    BRCA1-BARD1 E3 activity was found to be required for mitotic spindle-pole assembly and TPX2 accumulation, extending the complex's functions beyond interphase DNA repair.

    Evidence Xenopus egg extracts; RNAi in mammalian cells; E3-deficient mutant analysis; co-IP with TPX2/NuMA/XRHAMM

    PMID:17081976

    Open questions at the time
    • Direct ubiquitination substrates at spindle poles not identified
    • Relevance to human tumor suppression unclear
  10. 2007 High

    Crystal structures of the BARD1 ankyrin repeat and BRCT domains provided atomic-level understanding of two key chromatin-reading modules and explained effects of cancer-associated mutations.

    Evidence X-ray crystallography at 2.0 Å (ankyrin) and 1.9 Å (BRCT); structural mapping of cancer mutations

    PMID:17550235 PMID:18480049

    Open questions at the time
    • Ligands for each domain not yet identified
    • BRCT phosphopeptide-binding pocket appeared degenerate—functional significance unclear
  11. 2007 High

    BARD1 was found to translocate to mitochondria independently of BRCA1, where it induces Bax oligomerization and apoptosis, establishing a mitochondrial apoptotic function.

    Evidence Mitochondrial fractionation; immunofluorescence; YFP-BARD1 targeting; Bax oligomerization and apoptosis assays

    PMID:17510055

    Open questions at the time
    • Mechanism of BARD1 mitochondrial import unknown
    • Whether mitochondrial BARD1 contributes to tumor suppression in vivo not tested
  12. 2016 High

    BRCA1-BARD1 H2A ubiquitylation was shown to reposition 53BP1 via SMARCAD1 to promote resection and HR, solving how the complex antagonizes the anti-resection barrier.

    Evidence BARD1-deficient cell complementation with H2A-ubiquitin fusion; SMARCAD1 knockdown; 53BP1 repositioning assays

    PMID:27239795

    Open questions at the time
    • Whether SMARCAD1 is the sole reader of BRCA1-BARD1-generated H2A-ub not established
    • Mechanism of 53BP1 repositioning (eviction vs. spreading) unclear
  13. 2017 High

    Biochemical reconstitution showed BRCA1-BARD1 directly promotes RAD51-mediated synaptic complex assembly, establishing a catalytic role in the strand-invasion step of HDR beyond simple recruitment.

    Evidence In vitro reconstitution with purified proteins; RAD51-interaction mutants; cell-based HDR assays

    PMID:28976962

    Open questions at the time
    • Whether BARD1 or BRCA1 makes the primary RAD51 contact debated
    • Structural basis of RAD51 stimulation unknown
  14. 2018 High

    Separation-of-function BARD1 BRCT mutations in mice revealed that PAR-dependent recruitment to stalled forks protects replication forks independently of HDR, genetically uncoupling two major genome-maintenance functions.

    Evidence Bard1 BRCT knock-in mouse models; DNA fiber assays; PAR binding experiments; HR assays

    PMID:30244837

    Open questions at the time
    • How PAR binding by BARD1 BRCT is coordinated with PARP1 activity unclear
    • Whether fork protection function involves E3 activity not tested
  15. 2019 High

    BARD1 ankyrin repeat recognition of H4K20me0 was identified as the mechanism restricting BRCA1-BARD1 to post-replicative (sister chromatid) chromatin, explaining cell-cycle-dependent HR pathway choice.

    Evidence Biochemical binding assays; mutagenesis; DSB recruitment assays; PARP inhibitor sensitivity

    PMID:30804502

    Open questions at the time
    • Whether H4K20me0 reading is sufficient or requires cooperation with other marks not fully resolved
  16. 2019 High

    PIN1-mediated prolyl isomerization of BRCA1-BARD1 was shown to enhance RAD51 interaction at stalled forks, identifying a post-translational switch that potentiates fork protection distinctly from PALB2-mediated HDR.

    Evidence Cell-based fork protection (DNA fiber); co-IP; PIN1 inhibition; genetic variant analysis

    PMID:31270457

    Open questions at the time
    • Specific BARD1 proline residues isomerized not mapped
    • Structural basis of isomerization-enhanced RAD51 binding unknown
  17. 2021 High

    Cryo-EM structures of BRCA1-BARD1 on ubiquitinated nucleosomes, combined with identification of the BARD1 BUDR motif reading H2AK15ub, revealed the full multivalent nucleosome-recognition mechanism and how the RING heterodimer orients E2 for site-specific H2A C-terminal ubiquitylation.

    Evidence Cryo-EM structures (3.1 Å); biochemical binding and ubiquitylation assays; mutagenesis; genetic epistasis in mice

    PMID:33589814 PMID:34102105 PMID:34321663 PMID:34321665

    Open questions at the time
    • How BRCA1-BARD1 discriminates damaged vs. undamaged post-replicative nucleosomes in real time unclear
    • Dynamics of multivalent engagement not captured by static structures
  18. 2023 High

    Generation of truly ligase-null BRCA1-BARD1 variants revealed that E3 activity contributes to both DNA resection and later HDR completion stages, correcting prior conclusions drawn from hypomorphic mutants.

    Evidence In vitro ubiquitylation with full-length proteins; separation-of-function alleles; cell-based HDR and damage sensitivity

    PMID:37797621

    Open questions at the time
    • Specific late-stage HDR substrates of the E3 not identified
    • Whether ligase activity is required for fork protection not addressed
  19. 2024 High

    Full biochemical reconstitution demonstrated BRCA1-BARD1 directly stimulates all three long-range resection pathways (EXO1, DNA2-BLM, DNA2-WRN) and, in the presence of RAD51, switches to inhibiting DNA degradation, unifying its resection-promoting and fork-protective activities in a single mechanistic framework.

    Evidence Reconstitution with purified proteins; single-molecule analysis; mutagenesis; cell-based resection assays

    PMID:39261728 PMID:39261729

    Open questions at the time
    • How BRCA1-BARD1 senses RAD51 loading to switch from resection to fork protection not mechanistically resolved
    • BARD1 DNA-binding module structure not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Outstanding questions include how BRCA1-BARD1 transitions between its resection-promoting and fork-protective modes in real time, the structural basis for BARD1's standalone DNA-binding activity, the in vivo relevance and mechanism of BARD1's mitochondrial apoptotic function, and whether K6-linked ubiquitin chains have dedicated readers that mediate downstream signaling.
  • No structural model of BARD1 DNA-binding module
  • K6-ubiquitin chain readers unidentified
  • Mitochondrial apoptotic pathway not validated in genetic tumor models

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0016874 ligase activity 4 GO:0042393 histone binding 4 GO:0003677 DNA binding 3
Localization
GO:0005694 chromosome 5 GO:0005634 nucleus 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-73894 DNA Repair 8 R-HSA-392499 Metabolism of proteins 4 R-HSA-8953854 Metabolism of RNA 3 R-HSA-1640170 Cell Cycle 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-69306 DNA Replication 2
Partners
BAP1BRCA1CSTF2OLA1PIN1RAD51SIRT2SMARCAD1
Complex memberships
BRCA1-BARD1 heterodimerBRCA1-C complex (MRN-CtIP-BRCA1-BARD1)

Evidence

Reading pass · 55 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 The BRCA1-BARD1 heterodimeric RING finger complex functions as a ubiquitin ligase (E3); individually BRCA1 and BARD1 have very low ubiquitin ligase activities, but together they exhibit dramatically higher activity. The breast cancer-derived BRCA1(C61G) mutation, which disrupts BARD1 interaction, abolishes this activity. In vitro ubiquitin ligase assay with bacterially purified RING finger domains; mutagenesis; co-transfection stability assays The Journal of biological chemistry High 11278247
2001 Solution structure of the BRCA1-BARD1 RING-RING heterodimer determined by NMR, revealing the structural basis for heterodimerization and providing a model for ubiquitin ligase activity; comparison with RAG1 RING homodimer reveals structural diversity of RING-RING complexes. NMR solution structure determination Nature structural biology High 11573085
2003 UbcH5c (E2 ubiquitin-conjugating enzyme) binds exclusively to the BRCA1 RING domain (not BARD1 RING) within the BRCA1-BARD1 heterodimer; the binding interface involves the first and second Zn2+-loops and central alpha-helix of BRCA1 RING; UbcH7 also binds but is not active in ubiquitin ligase assays, demonstrating binding alone is insufficient for activity. NMR spectroscopy mapping; site-directed mutagenesis; in vitro ubiquitin ligase activity assays Proceedings of the National Academy of Sciences of the United States of America High 12732733
2017 BRCA1-BARD1 directly promotes RAD51-mediated homologous DNA pairing by enhancing assembly of the synaptic complex; both BRCA1 and BARD1 bind DNA and interact with RAD51; BRCA1-BARD1 mutants with weakened RAD51 interactions show compromised DNA joint formation and impaired HDR in cells. In vitro biochemical reconstitution with purified proteins; mutagenesis; cell-based HDR assays Nature High 28976962
2016 BRCA1-BARD1 ubiquitin ligase activity ubiquitinates H2A and is required for repositioning 53BP1 on damaged chromatin to promote DNA resection and homologous recombination; this function requires the chromatin remodeler SMARCAD1, which binds H2A-ubiquitin via its CUE domains. Cell-based assays; BARD1-deficient cell complementation with H2A-ubiquitin fusion; SMARCAD1 knockdown; 53BP1 repositioning assays Nature structural & molecular biology High 27239795
2019 The ankyrin repeat domain of BARD1 acts as a reader of unmethylated histone H4 lysine 20 (H4K20me0) on post-replicative chromatin; BARD1 ankyrin repeat mutations disabling H4K20me0 recognition abrogate BRCA1 accumulation at DSBs, causing aberrant 53BP1 build-up and impairing homologous recombination. Biochemical binding assays; cell-based DSB recruitment assays; mutagenesis; PARP inhibitor sensitivity assays Nature cell biology High 30804502
2021 BARD1 contains a tandem BRCT-domain-associated ubiquitin-dependent recruitment motif (BUDR) that directly engages RNF168-generated H2AK15ub to recruit BRCA1 to DSBs; BARD1 binds nucleosomes through multivalent interactions coordinating H2AK15ub recognition (BUDR) and H4K20me0 recognition (ankyrin repeat domain); genetic epistasis shows BARD1 chromatin-binding activity can be relieved by RNF168 or 53BP1 deletion. Biochemical binding assays; cell-based recruitment assays; mutagenesis; genetic epistasis in cells Nature High 34321663
2021 Cryo-EM structure of BRCA1-BARD1 bound to nucleosome shows BARD1 ankyrin repeat and tandem BRCT domains bind nucleosomal histones, DNA, and monoubiquitin at H2A K13/K15 (DSB-specific marks); RING domains orient E2 ubiquitin-conjugating enzyme atop the nucleosome for ubiquitin transfer to H2A/H2AX C-terminal tails; recognition of monoubiquitin by BRCA1-BARD1 at H2A N-terminus blocks polyubiquitin chain formation and promotes ubiquitylation at H2A C-terminus. Cryo-electron microscopy structure determination; biochemical ubiquitylation assays Nature High 34321665
2021 Cryo-EM structure of BARD1 bound to ubiquitinated nucleosome core particle at 3.1 Å; BARD1 simultaneously recognizes H2AK15ub (damage-induced) and H4K20me0 (replication-associated); multiple disease-causing BARD1 mutations disrupt BARD1-nucleosome interactions and impair HR. Cryo-EM structure; in vitro and in vivo HR assays; mutagenesis Molecular cell High 34102105
2021 BRCA1/BARD1 site-specific ubiquitylation of nucleosomal H2A is directed by a novel BARD1-histone interface that targets lysines 125, 127, and 129 in the H2A C-terminal tail, distinct from PRC1's targeting of H2A K119; NMR reveals E3-mediated substrate regulation through modulation of dynamics in the H2A C-terminal tail. Cryo-EM structure of RING heterodimer-UbcH5c-nucleosome complex; NMR; biochemical ubiquitylation assays; mutagenesis Nature structural & molecular biology High 33589814
2006 BRCA1/BARD1 is required for mitotic spindle-pole assembly and for accumulation of TPX2 on spindle poles; this function is centrosome-independent, operates downstream of Ran GTPase, and depends on BRCA1/BARD1 E3 ubiquitin ligase activity; Xenopus BRCA1/BARD1 forms complexes with TPX2, NuMA, and XRHAMM, and specifically attenuates XRHAMM function. Xenopus egg extracts; RNAi knockdown in mammalian cells; co-immunoprecipitation; ubiquitin ligase-deficient mutant analysis Cell High 17081976
2019 BRCA1-BARD1-dependent replication fork protection requires PIN1-mediated prolyl isomerization of BRCA1-BARD1, which enhances the complex's interaction with RAD51, increasing RAD51 presence at stalled replication structures; this is distinct from the canonical BRCA1-PALB2 interaction required for HDR. Cell-based fork protection assays (DNA fiber); co-immunoprecipitation; PIN1 inhibition; genetic variants analysis Nature High 31270457
2024 BRCA1-BARD1 directly promotes long-range DNA end resection by EXO1 and DNA2 nuclease pathways; in the DNA2-dependent pathway, BRCA1-BARD1 stimulates DNA unwinding by Werner or Bloom helicase; together with MRE11-RAD50-NBS1 and phospho-CtIP, BRCA1-BARD1 forms the BRCA1-C complex that synergistically stimulates resection; in the presence of RAD51, BRCA1-BARD1 switches to inhibiting DNA degradation (fork protection). Biochemical reconstitution with purified proteins; single-molecule analysis; mutagenesis Nature High 39261728
2024 BRCA1-BARD1 physically interacts with EXO1, BLM, and WRN and upregulates all three long-range DNA end resection pathways; BARD1 harbors a stand-alone DNA-binding module essential for end resection both in vitro and in cells. Reconstituted biochemical systems with highly purified proteins; single-molecule assays; mutagenesis; cell-based resection assays Nature High 39261729
2001 BARD1 interacts with the polyadenylation factor CstF-50, and this interaction inhibits mRNA 3' cleavage/polyadenylation in vitro; following DNA damage (hydroxyurea or UV), increased CstF/BARD1/BRCA1 complex is detected; the tumor-associated BARD1 mutation Q564H reduces CstF binding and abrogates polyadenylation inhibition. In vitro polyadenylation assay; co-immunoprecipitation; cell extracts from DNA-damaged cells; mutagenesis Cell High 11257228
1999 BARD1 interacts with polyadenylation factor CstF-50 both in vitro and in intact cells; this interaction inhibits polyadenylation in vitro; BARD1 also interacts with RNA polymerase II. In vitro binding assay; co-immunoprecipitation; in vitro polyadenylation inhibition assay Science (New York, N.Y.) High 10477523
2005 BRCA1/BARD1 ubiquitin ligase directly ubiquitinates the elongating (hyperphosphorylated) form of RNA polymerase II (RNAP IIO), specifically the Ser-5 phosphorylated form of Rpb1; siRNA knockdown of BRCA1 and BARD1 stabilizes RNAP II after DNA damage and reverts inhibition of mRNA 3' cleavage; BRCA1/BARD1 thereby promotes degradation of stalled RNAP IIO to inhibit coupled transcription-RNA processing. In vitro ubiquitylation assay; siRNA knockdown; cell-based RNAP II ubiquitination; in vitro 3' cleavage assay Genes & development High 15905410
2005 BRCA1/BARD1 ubiquitinates the Ser-5 hyperphosphorylated form of Rpb1 (largest subunit of RNAP II); overexpression of BRCA1 in cells stimulates DNA damage-induced Rpb1 ubiquitination; the BRCA1 C-terminus is required for efficient Rpb1 ubiquitination in cells but dispensable in vitro. In vitro ubiquitylation assay; cell-based ubiquitination upon DNA damage; BRCA1 deletion mutant analysis The Journal of biological chemistry High 15886201
2002 The BRCA1/BARD1 complex promotes monoubiquitination of histone H2A/H2AX and exhibits autoubiquitination with non-K48-linked polyubiquitin chain assembly; BRCA1/BARD1 is associated with polyubiquitin chains in vivo; these non-K48 chains may form a signaling platform for DNA repair. In vitro ubiquitylation assay; bacterial co-expression; co-immunoprecipitation in transfected cells; K48A/K63A ubiquitin mutants The Journal of biological chemistry High 11927591
2004 BRCA1:BARD1 catalyzes the formation of K6-linked polyubiquitin conjugates at DNA replication structures in S-phase and at DSB repair sites after ionizing radiation; siRNA depletion of endogenous BRCA1:BARD1 abrogates these ubiquitin conjugation foci; expression of K6-mutant ubiquitin inhibits focus formation. Immunofluorescence; siRNA knockdown; K6 ubiquitin mutant expression; cell-based assays Human molecular genetics High 14976165
2002 BARD1 promotes nuclear import of BRCA1 via the BRCA1 RING domain, and masks the BRCA1 nuclear export signal, causing nuclear retention; loss of BARD1 interaction shifts BRCA1 to the cytoplasm; BARD1 promotes formation of DNA damage-induced nuclear foci. Transfection of BRCA1/BARD1 mutants; fluorescence microscopy; nuclear fractionation; siRNA The Journal of biological chemistry High 11925436
2002 Enhancement of BRCA1 E3 ubiquitin ligase activity by BARD1 depends on direct protein-protein interaction; BARD1 stimulates both K48- and K63-linked polyubiquitin chain formation, predominantly K63; co-expression of BRCA1 and BARD1 increases the abundance and stability of both proteins, dependent on heterodimerization. In vitro ubiquitylation assay; mutagenesis; K48A/K63A ubiquitin mutants; co-expression stability assays The Journal of biological chemistry High 12431996
2004 Nucleophosmin/B23 (NPM) is identified as a substrate of the BRCA1-BARD1 ubiquitin ligase; NPM interacts with N-terminal fragments of BRCA1 and BARD1 in a heterodimer-dependent manner; BRCA1-BARD1 catalyzes NPM polyubiquitination in vitro and in vivo, leading to NPM stabilization rather than degradation. Mass spectrometry substrate identification; in vitro ubiquitylation assay; co-immunoprecipitation; in vivo ubiquitination The Journal of biological chemistry High 15184379
2006 Following genotoxic stress, BRCA1/BARD1 forms two distinct DNA damage-dependent super-complexes with TopBP1 and Mre11/Rad50/NBS1 respectively; these interactions are dependent on specific checkpoint kinases; each super-complex contributes to a distinctive aspect of the DNA damage response. Co-immunoprecipitation after DNA damage; checkpoint kinase inhibition; functional assays Genes & development High 16391231
2004 BRCA1-BARD1 complexes are required for ATM/ATR-mediated phosphorylation of p53 at Ser-15 following IR- and UV-induced DNA damage; prior ATM/ATR-dependent phosphorylation of BRCA1 at Ser-1423 or Ser-1524 regulates the ability of ATM/ATR to phosphorylate p53(Ser-15); this is required for G1/S checkpoint arrest via p21 induction. siRNA depletion of BRCA1 and BARD1; phospho-specific western blotting; cell cycle analysis The Journal of biological chemistry High 15159397
2009 BAP1 (ubiquitin C-terminal hydrolase) interacts with BARD1 RING domain (residues 182-365) and inhibits BRCA1/BARD1 E3 ligase activity by interfering with BRCA1-BARD1 association; BAP1 can deubiquitinate BRCA1/BARD1-catalyzed polyubiquitin chains in vitro, but a catalytically inactive BAP1 mutant (C91S) still inhibits ubiquitination, indicating a second steric mechanism; BAP1 knockdown causes IR hypersensitivity. Surface plasmon resonance (BIAcore); in vitro ubiquitylation assay; catalytically inactive mutant; shRNA knockdown Cancer research High 19117993
2005 CDK2-cyclin A1/E1 phosphorylates BARD1 at its N-terminus (S148, S251, S288, T299) in vivo and in vitro; CDK2-cyclin E1 co-expression dramatically disrupts BRCA1-BARD1-mediated ubiquitination of NPM and BRCA1 autoubiquitination; CDK2 inhibition of ligase activity acts through promoting cytoplasmic export rather than direct phosphorylation of the catalytic interface. In vitro kinase assay; cell-based ubiquitination assay; CDK2 co-expression; nuclear-cytoplasmic fractionation Cancer research High 15665273
2003 Expression of truncated BARD1 peptides capable of interacting with Brca1 causes a homologous recombination repair deficiency in cells; this effect is severe in cells harboring a Brca1 splice product deleted for exon 11, demonstrating BARD1 participates with BRCA1 in HDR of chromosome breaks. Cell-based HDR assay (I-SceI); expression of dominant-negative BARD1 truncations Molecular and cellular biology High 14560035
2018 BARD1 RING domain is critical for BRCA1/BARD1 binding to nucleosomes and ubiquitylation of histone H2A; cancer-predisposing BARD1 missense mutations in the RING domain (Cys53Trp, Cys71Tyr, Cys83Arg) retain heterodimerization with BRCA1 but are deficient in nucleosome binding and H2A ubiquitylation, and cause loss of transcriptional repression of estrogen metabolism genes CYP1A1 and CYP3A4. In vitro nucleosome-binding assays; in vitro H2A ubiquitylation; gene editing of BARD1 in breast epithelial cells; RT-qPCR of CYP genes Proceedings of the National Academy of Sciences of the United States of America High 29367421
2021 RNF168-generated H2AK15ub recruits BARD1 through its BRCT-domain BUDR motif; subsequently BARD1-BRCA1 accumulates PALB2-RAD51 at DNA breaks via the CC domain-mediated BRCA1-PALB2 interaction; genetic epistasis in mice shows that Rnf168 and Brca1CC alleles interact to disrupt development and reduce Palb2-Rad51 localization. Epistasis in mice (Rnf168/Brca1CC double mutant); cell-based localization assays; mechanistic binding experiments Nature communications High 34408138
2023 BRCA1-BARD1 E3 ligase activity is required not only for DNA resection during HDR but also contributes to later stages of HDR completion; a truly ligase-null variant and a variant specifically impaired in targeting nucleosomal histones both cause hypersensitivity to DNA-damaging agents; previous BRCA1-BARD1 mutants used as 'ligase-dead' retain significant residual activity. In vitro ubiquitylation assay with full-length proteins; separation-of-function alleles; cell-based HDR and DNA damage sensitivity assays Molecular cell High 37797621
2004 BARD1 has a CRM1-dependent nuclear export signal (NES) near its N-terminal RING domain; BRCA1 co-expression masks the NES and retains BARD1 in the nucleus; BARD1 apoptotic activity is stimulated by nuclear export, and siRNA-mediated silencing of BRCA1 or disruption of the BARD1/BRCA1 interaction increases cytoplasmic BARD1 and apoptosis. CRM1 inhibitor (leptomycin B); fluorescence microscopy; siRNA; peptide competition; flow cytometry for apoptosis Oncogene High 14647430
2001 BARD1 mediates apoptosis in a BRCA1-independent manner; overexpression of BARD1 induces apoptosis; the proapoptotic activity involves binding to and stabilization of p53; BARD1-repressed cells are defective for the apoptotic response to genotoxic stress; the tumor-associated Q564H mutation is defective in apoptosis induction. BARD1 overexpression; BARD1 repression (antisense/ribozyme); co-immunoprecipitation with p53; apoptosis assays Molecular cell High 11779501
2005 BARD1 induces p53 stability and apoptosis by binding to Ku-70 (regulatory subunit of DNA-PK) and unphosphorylated/Ser-15-phosphorylated p53, catalyzing p53 phosphorylation on Ser-15; upregulation of BARD1 alone is sufficient for p53 stabilization and Ser-15 phosphorylation. Co-immunoprecipitation; overexpression of BARD1; phospho-specific western blotting; apoptosis assays in NuTu-19 cells Oncogene Medium 15782130
2007 BARD1 localizes to mitochondria (detected by immunofluorescence and fractionation); translocation to mitochondria is stimulated by DNA damage and does not require BRCA1; ectopic BARD1 at mitochondria induces apoptosis, loss of mitochondrial membrane potential, and Bax oligomerization; the cancer-associated DeltaRIN splice variant is recruited to mitochondria but does not stimulate apoptosis. Immunofluorescence microscopy; mitochondrial fractionation/immunoblotting; YFP-BARD1 expression; apoptosis and Bax oligomerization assays The Journal of biological chemistry High 17510055
1997 BARD1 colocalizes with BRCA1 in nuclear dots during S phase but not G1 phase; BARD1 is exclusively nuclear in both G1 and S phase cells; progression to S phase triggers aggregation of nuclear BARD1 into BRCA1 nuclear dots, indicating cell cycle-dependent co-localization. Immunofluorescence and cell fractionation; cell cycle synchronization Proceedings of the National Academy of Sciences of the United States of America High 9342365
2015 BARD1 BRCT domain interacts with HP1γ via a conserved HP1-binding motif; this interaction is mediated through H3K9me2 in an ATM-dependent, RNF168-independent manner and is required for retention of BARD1, BRCA1, and CtIP at DSB sites; disruption allows ectopic accumulation of RIF1 at damage sites in S-phase. Co-immunoprecipitation; in vitro pulldown; laser-induced damage recruitment assays; HP1 depletion; ATM inhibition Cancer research High 25634209
2020 The lncRNA BGL3 binds PARP1 and BARD1 (specifically the BARD1 C-terminal BRCT domain and residues 127-424); BGL3 is recruited to DSBs by PARP1 and mediates retention of BRCA1/BARD1 at DSBs by enabling interaction of BRCA1/BARD1 with HP1γ and RAD51; BGL3 depletion causes genomic instability and DNA damage sensitivity. RNA antisense purification with quantitative MS (RAP-qMS); co-immunoprecipitation; cell-based DSB retention assays The EMBO journal Medium 32347575
2013 OLA1 (Obg-like ATPase 1) interacts with the C-terminal region of BARD1 and the N-terminal region of BRCA1 and γ-tubulin; OLA1 localizes to centrosomes in interphase and spindle poles in mitosis; OLA1 knockdown causes centrosome amplification and microtubule aster formation; a breast cancer-derived OLA1 mutant E168Q fails to bind BRCA1 and rescue these defects. Mass spectrometry; co-immunoprecipitation; immunofluorescence; siRNA knockdown; mutagenesis Molecular cell High 24289923
2009 Full-length BARD1 colocalizes with Aurora B at the midbody, mediates Aurora B ubiquitination and degradation; the cancer-associated BARD1β isoform instead scaffolds Aurora B and BRCA2; selective siRNA depletion of full-length BARD1 causes massive Aurora B upregulation. Selective siRNA; co-immunoprecipitation; immunofluorescence; cell growth assays Cancer research Medium 19176389
2021 SIRT2 deacetylase complexes with BRCA1-BARD1 and deacetylates conserved lysines in the BARD1 RING domain at the BRCA1-BARD1 interface, promoting heterodimerization, mutual protein stability, nuclear retention, and localization to DNA damage sites, thereby facilitating efficient HR. Co-immunoprecipitation; deacetylation assays; SIRT2 knockdown/knockout; cell-based HR assays; nuclear fractionation Cell reports High 33789098
2018 The BARD1 BRCT domain (not the BRCA1 BRCT domain) recruits BRCA1/BARD1 to stalled replication forks in a poly(ADP-ribose)-dependent manner; Bard1 BRCT mutations (S563F, K607A) abolish PAR-dependent fork recruitment and cause fork degradation and chromosomal instability without affecting HDR; this separates the fork protection and HDR functions of BARD1. Mouse models (Bard1S563F, Bard1K607A, Brca1S1598F knock-in); DNA fiber assays; HR assays; PAR binding experiments Molecular cell High 30244837
2003 Bard1-null mice die between E7.5 and E8.5 due to severe impairment of cell proliferation; in the absence of p53, lethality is delayed to E9.5; Bard1 mutant cells show increased chromosomal aneuploidy; the nearly identical phenotypes of Bard1-null, Brca1-null, and double Bard1/Brca1-null mice provide genetic evidence that developmental functions of Brca1 and Bard1 are mediated through the Brca1/Bard1 heterodimer. Mouse knockout; embryonic phenotyping; chromosomal analysis; p53-null epistasis Molecular and cellular biology High 12832489
2008 Conditional inactivation of Bard1 or Brca1 in mammary epithelial cells produces indistinguishable basal-like breast carcinomas; double Bard1/Brca1 conditional mutants develop the same tumors, providing genetic evidence that tumor suppressor activities of both genes are mediated through the BRCA1/BARD1 heterodimer. Conditional knockout mouse models; histopathology; cytogenetics Proceedings of the National Academy of Sciences of the United States of America High 18443292
2007 Ankyrin and BRCT motifs of BARD1 are each essential for both chromosome stability and HDR; cancer-associated missense mutations in the BRCT domains (C557S, Q564H, V695L, S761N) do not affect HDR activity of BARD1; synthetic mutations predicted to ablate BRCT phospho-recognition activity do not perturb HDR, suggesting BRCT domain HDR function is phosphopeptide-recognition independent. Complementation of Bard1-null mouse mammary carcinoma cells; I-SceI HDR assay; mutagenesis The Journal of biological chemistry High 17848578
2009 Ligand-free LXRα interacts with BARD1/BRCA1, which promotes its ubiquitination and degradation; LXR ligand represses ubiquitination and degradation of LXRα by inhibiting the LXRα-BARD1 interaction; overexpression of BARD1/BRCA1 promotes ubiquitination of LXRα and reduces its recruitment to target gene promoters. Co-immunoprecipitation; ubiquitination assay; BARD1 knockdown; LXR ligand treatment; ChIP Molecular endocrinology (Baltimore, Md.) Medium 19164445
2007 Crystal structure of the BARD1 ankyrin repeat domain at 2.0 Å resolution; the domain contains four ankyrin repeats with a non-canonical C-terminal capping repeat and conserved acidic surface features; cancer-associated mutations N470S and V507M do not cause observable structural defects. X-ray crystallography The Journal of biological chemistry High 18480049
2007 Crystal structure of the BARD1 BRCT domains at 1.9 Å reveals a phosphoserine-binding pocket (P1) similar to BRCA1 and MDC1 BRCT domains; the P2 selectivity pocket contains distinctive histidines (His685, His686) that may regulate ligand recognition in a pH-dependent manner; structural basis for cancer mutations C645R, V695L, and S761N explained. X-ray crystallography; structural analysis of cancer mutations Biochemistry High 17550235
2008 The BARD1 C-terminal region mediates CstF-50 interaction through the ankyrin-BRCT linker region (not the ankyrin or BRCT domains themselves); the crystal structure of the BARD1 BRCT domain reveals a degenerate phosphopeptide binding pocket; SAXS and limited proteolysis show ankyrin and BRCT domains are linked by a flexible tether without fixed relative orientation. Protein pulldown with deletion mutants; crystal structure; small-angle X-ray scattering (SAXS); limited proteolysis Biochemistry High 18842000
2006 BARD1 enhances BRCA1 DNA binding in a ubiquitination-dependent and independent manner; BARD1 itself cannot directly bind DNA; autoubiquitination of BRCA1/BARD1 heterodimers further enhances DNA binding affinity; the C-terminus of BRCA1 contributes to heterodimer stability beyond the N-terminal RING domains. In vitro DNA-binding assays (EMSAs); ubiquitination-deficient BRCA1 mutants; deletion analysis Cancer research Medium 16489000
2002 BARD1 is a component of the RNA polymerase II holoenzyme complex; the BRCA1 N-terminus (bound by BARD1) is required for >98% of BRCA1 association with the holo-pol; the BRCA1 N-terminus is also required for nuclear dot formation in S-phase. Co-immunoprecipitation with RNA pol II holoenzyme; BRCA1 deletion mutant analysis; immunocytochemistry Cancer research Medium 12154023
2012 Common variation at BARD1 correlates with increased expression of the oncogenic BARD1β isoform in neuroblastoma; BARD1β is sufficient for neoplastic transformation of murine fibroblasts; BARD1β stabilizes Aurora kinases in neuroblastoma cells. siRNA silencing of BARD1β; neoplastic transformation assay; Aurora kinase co-immunoprecipitation/immunoblotting Cancer research Medium 22350409
2004 In C. elegans, the BARD1 ortholog Ce-BRD-1 interacts with components of the sumoylation pathway and TACC domain protein TAC-1; depletion of Ce-brd-1 phenocopies Ce-brc-1 depletion (elevated p53-dependent germ cell death, radiation sensitivity, high incidence of males), supporting a shared role in DNA repair. Protein interaction screens (yeast two-hybrid/co-IP); RNAi depletion; radiation sensitivity assays in C. elegans Current biology : CB Medium 14711411
2001 Xenopus BARD1 and BRCA1 form functional heterodimers; depleting either BARD1 or BRCA1 from frog embryos causes similar developmental defects and depletion of the other protein due to decreased stability; each protein controls the abundance, stability, and function of the other in a heterodimerization-dependent manner. Xenopus developmental depletion; co-immunoprecipitation; protein stability analysis Proceedings of the National Academy of Sciences of the United States of America High 11593018
2011 p53 associates with BARD1 and CstF1 in UV-treated cell extracts; p53 inhibits mRNA 3' cleavage in vitro; a tumor-associated p53 mutation decreases interaction with BARD1 and CstF and decreases UV-induced inhibition of 3' processing; p53 expression levels inversely correlate with mRNA 3' cleavage levels. Co-immunoprecipitation from UV-treated cell extracts; in vitro 3' cleavage assay; p53 mutant analysis; RT-qPCR Oncogene Medium 21383700

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 The RING heterodimer BRCA1-BARD1 is a ubiquitin ligase inactivated by a breast cancer-derived mutation. The Journal of biological chemistry 555 11278247
2001 Structure of a BRCA1-BARD1 heterodimeric RING-RING complex. Nature structural biology 433 11573085
2015 Germline Mutations in the BRIP1, BARD1, PALB2, and NBN Genes in Women With Ovarian Cancer. Journal of the National Cancer Institute 325 26315354
2017 BRCA1-BARD1 promotes RAD51-mediated homologous DNA pairing. Nature 299 28976962
2003 Binding and recognition in the assembly of an active BRCA1/BARD1 ubiquitin-ligase complex. Proceedings of the National Academy of Sciences of the United States of America 299 12732733
2020 The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication. Nature reviews. Molecular cell biology 271 32094664
2006 Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1-containing complexes. Genes & development 260 16391231
2016 Human BRCA1-BARD1 ubiquitin ligase activity counteracts chromatin barriers to DNA resection. Nature structural & molecular biology 227 27239795
2006 The BRCA1/BARD1 heterodimer modulates ran-dependent mitotic spindle assembly. Cell 227 17081976
2004 BRCA1 : BARD1 induces the formation of conjugated ubiquitin structures, dependent on K6 of ubiquitin, in cells during DNA replication and repair. Human molecular genetics 223 14976165
2002 Autoubiquitination of the BRCA1*BARD1 RING ubiquitin ligase. The Journal of biological chemistry 182 11927591
2009 BRCA1-associated protein 1 interferes with BRCA1/BARD1 RING heterodimer activity. Cancer research 179 19117993
2001 The BARD1-CstF-50 interaction links mRNA 3' end formation to DNA damage and tumor suppression. Cell 179 11257228
2002 Enhancement of BRCA1 E3 ubiquitin ligase activity through direct interaction with the BARD1 protein. The Journal of biological chemistry 172 12431996
2002 BARD1 induces BRCA1 intranuclear foci formation by increasing RING-dependent BRCA1 nuclear import and inhibiting BRCA1 nuclear export. The Journal of biological chemistry 162 11925436
2019 H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids. Nature cell biology 161 30804502
1998 Mutations in the BRCA1-associated RING domain (BARD1) gene in primary breast, ovarian and uterine cancers. Human molecular genetics 154 9425226
1997 Cell cycle-dependent colocalization of BARD1 and BRCA1 proteins in discrete nuclear domains. Proceedings of the National Academy of Sciences of the United States of America 151 9342365
1999 Functional interaction of BRCA1-associated BARD1 with polyadenylation factor CstF-50. Science (New York, N.Y.) 145 10477523
2021 BARD1 reads H2A lysine 15 ubiquitination to direct homologous recombination. Nature 140 34321663
2005 BRCA1/BARD1 inhibition of mRNA 3' processing involves targeted degradation of RNA polymerase II. Genes & development 126 15905410
2004 BRCA1/BARD1 orthologs required for DNA repair in Caenorhabditis elegans. Current biology : CB 124 14711411
2001 Functional communication between endogenous BRCA1 and its partner, BARD1, during Xenopus laevis development. Proceedings of the National Academy of Sciences of the United States of America 124 11593018
1999 Mapping the functional domains of BRCA1. Interaction of the ring finger domains of BRCA1 and BARD1. The Journal of biological chemistry 124 10026184
2005 BRCA1/BARD1 ubiquitinate phosphorylated RNA polymerase II. The Journal of biological chemistry 123 15886201
2004 BRCA1-BARD1 complexes are required for p53Ser-15 phosphorylation and a G1/S arrest following ionizing radiation-induced DNA damage. The Journal of biological chemistry 118 15159397
2004 Nucleophosmin/B23 is a candidate substrate for the BRCA1-BARD1 ubiquitin ligase. The Journal of biological chemistry 117 15184379
2018 Tamoxifen-resistant breast cancer cells are resistant to DNA-damaging chemotherapy because of upregulated BARD1 and BRCA1. Nature communications 113 29686231
2003 Loss of Bard1, the heterodimeric partner of the Brca1 tumor suppressor, results in early embryonic lethality and chromosomal instability. Molecular and cellular biology 111 12832489
2021 Mechanisms of BRCA1-BARD1 nucleosome recognition and ubiquitylation. Nature 107 34321665
2019 Isomerization of BRCA1-BARD1 promotes replication fork protection. Nature 107 31270457
2008 The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression. Proceedings of the National Academy of Sciences of the United States of America 104 18443292
2006 Is there more to BARD1 than BRCA1? Nature reviews. Cancer 99 16633366
2003 BARD1 participates with BRCA1 in homology-directed repair of chromosome breaks. Molecular and cellular biology 93 14560035
2012 Germline mutations in the DNA damage response genes BRCA1, BRCA2, BARD1 and TP53 in patients with therapy related myeloid neoplasms. Journal of medical genetics 92 22652532
2001 Identification of BARD1 as mediator between proapoptotic stress and p53-dependent apoptosis. Molecular cell 92 11779501
1998 In vitro repression of Brca1-associated RING domain gene, Bard1, induces phenotypic changes in mammary epithelial cells. The Journal of cell biology 86 9832560
2012 Common variation at BARD1 results in the expression of an oncogenic isoform that influences neuroblastoma susceptibility and oncogenicity. Cancer research 81 22350409
2015 Interaction of BARD1 and HP1 Is Required for BRCA1 Retention at Sites of DNA Damage. Cancer research 79 25634209
2011 Cancer predisposing BARD1 mutations in breast-ovarian cancer families. Breast cancer research and treatment 75 21344236
2004 Nuclear-cytoplasmic shuttling of BARD1 contributes to its proapoptotic activity and is regulated by dimerization with BRCA1. Oncogene 71 14647430
2021 Structural insight into BRCA1-BARD1 complex recruitment to damaged chromatin. Molecular cell 69 34102105
2009 Distinct roles of BARD1 isoforms in mitosis: full-length BARD1 mediates Aurora B degradation, cancer-associated BARD1beta scaffolds Aurora B and BRCA2. Cancer research 67 19176389
2005 BARD1 induces apoptosis by catalysing phosphorylation of p53 by DNA-damage response kinase. Oncogene 67 15782130
2021 BRCA1/BARD1 site-specific ubiquitylation of nucleosomal H2A is directed by BARD1. Nature structural & molecular biology 66 33589814
2018 The BRCT Domains of the BRCA1 and BARD1 Tumor Suppressors Differentially Regulate Homology-Directed Repair and Stalled Fork Protection. Molecular cell 65 30244837
2022 Moderate penetrance genes complicate genetic testing for breast cancer diagnosis: ATM, CHEK2, BARD1 and RAD51D. Breast (Edinburgh, Scotland) 64 35772246
2005 Regulation of BRCA1, BRCA2 and BARD1 intracellular trafficking. BioEssays : news and reviews in molecular, cellular and developmental biology 62 16108063
2013 The BRCA1/BARD1-interacting protein OLA1 functions in centrosome regulation. Molecular cell 61 24289923
2015 New concepts on BARD1: Regulator of BRCA pathways and beyond. The international journal of biochemistry & cell biology 60 26738429
2012 Replication of neuroblastoma SNP association at the BARD1 locus in African-Americans. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 60 22328350
2022 Enhancing the BOADICEA cancer risk prediction model to incorporate new data on RAD51C, RAD51D, BARD1 updates to tumour pathology and cancer incidence. Journal of medical genetics 57 36162851
2021 RNF168-mediated localization of BARD1 recruits the BRCA1-PALB2 complex to DNA damage. Nature communications 55 34408138
2008 Mutation of Arabidopsis BARD1 causes meristem defects by failing to confine WUSCHEL expression to the organizing center. The Plant cell 53 18591352
2019 MiR-210-3p protects endometriotic cells from oxidative stress-induced cell cycle arrest by targeting BARD1. Cell death & disease 52 30760709
2006 BRCA1 DNA-binding activity is stimulated by BARD1. Cancer research 52 16489000
2007 Crystal structure of the BARD1 BRCT domains. Biochemistry 51 17550235
2006 The BARD1 Cys557Ser variant and breast cancer risk in Iceland. PLoS medicine 51 16768547
2018 BRCA1-BARD1 associate with the synaptonemal complex and pro-crossover factors and influence RAD-51 dynamics during Caenorhabditis elegans meiosis. PLoS genetics 50 30383754
2018 Fine mapping of 2q35 high-risk neuroblastoma locus reveals independent functional risk variants and suggests full-length BARD1 as tumor-suppressor. International journal of cancer 49 30132831
2004 Nuclear-cytoplasmic translocation of BARD1 is linked to its apoptotic activity. Oncogene 49 15077185
2019 Germline loss-of-function variants in the BARD1 gene are associated with early-onset familial breast cancer but not ovarian cancer. Breast cancer research : BCR 48 31036035
2006 A homologue of the breast cancer-associated gene BARD1 is involved in DNA repair in plants. The EMBO journal 48 16957774
2017 BARD1 Gene Polymorphisms Confer Nephroblastoma Susceptibility. EBioMedicine 46 28161399
2005 Down-regulation of BRCA1-BARD1 ubiquitin ligase by CDK2. Cancer research 46 15665273
2018 BARD1 is necessary for ubiquitylation of nucleosomal histone H2A and for transcriptional regulation of estrogen metabolism genes. Proceedings of the National Academy of Sciences of the United States of America 45 29367421
2018 The tumor suppressor BRCA1-BARD1 complex localizes to the synaptonemal complex and regulates recombination under meiotic dysfunction in Caenorhabditis elegans. PLoS genetics 45 30383767
2011 BARD1: an independent predictor of survival in non-small cell lung cancer. International journal of cancer 45 21815143
2002 The BRCA1 and BARD1 association with the RNA polymerase II holoenzyme. Cancer research 45 12154023
2007 Structural requirements for the BARD1 tumor suppressor in chromosomal stability and homology-directed DNA repair. The Journal of biological chemistry 44 17848578
2002 Interaction of the EWS NH2 terminus with BARD1 links the Ewing's sarcoma gene to a common tumor suppressor pathway. Cancer research 44 12183411
2021 The BRCA1/BARD1 ubiquitin ligase and its substrates. The Biochemical journal 42 34591954
2020 BGL3 lncRNA mediates retention of the BRCA1/BARD1 complex at DNA damage sites. The EMBO journal 42 32347575
2017 Dualistic Role of BARD1 in Cancer. Genes 42 29292755
2024 Mechanism of BRCA1-BARD1 function in DNA end resection and DNA protection. Nature 41 39261728
2008 Crystal structure of the BARD1 ankyrin repeat domain and its functional consequences. The Journal of biological chemistry 37 18480049
2007 BARD1 translocation to mitochondria correlates with Bax oligomerization, loss of mitochondrial membrane potential, and apoptosis. The Journal of biological chemistry 37 17510055
2020 Literature Review of BARD1 as a Cancer Predisposing Gene with a Focus on Breast and Ovarian Cancers. Genes 36 32726901
2006 BARD1 variants Cys557Ser and Val507Met in breast cancer predisposition. European journal of human genetics : EJHG 35 16333312
2012 Expression of oncogenic BARD1 isoforms affects colon cancer progression and correlates with clinical outcome. British journal of cancer 34 22814582
2022 BARD1 mystery: tumor suppressors are cancer susceptibility genes. BMC cancer 33 35650591
2021 SIRT2 promotes BRCA1-BARD1 heterodimerization through deacetylation. Cell reports 33 33789098
2001 Identification of residues required for the interaction of BARD1 with BRCA1. The Journal of biological chemistry 33 11773071
2016 Expression of an Oncogenic BARD1 Splice Variant Impairs Homologous Recombination and Predicts Response to PARP-1 Inhibitor Therapy in Colon Cancer. Scientific reports 32 27197561
2011 p53 inhibits mRNA 3' processing through its interaction with the CstF/BARD1 complex. Oncogene 32 21383700
1998 Conservation of function and primary structure in the BRCA1-associated RING domain (BARD1) protein. Oncogene 32 9798686
2009 Liver X receptor ligands suppress ubiquitination and degradation of LXRalpha by displacing BARD1/BRCA1. Molecular endocrinology (Baltimore, Md.) 31 19164445
2006 Ubiquitination and proteasome-mediated degradation of BRCA1 and BARD1 during steroidogenesis in human ovarian granulosa cells. Molecular endocrinology (Baltimore, Md.) 31 17185394
2023 Crucial roles of the BRCA1-BARD1 E3 ubiquitin ligase activity in homology-directed DNA repair. Molecular cell 29 37797621
2017 Tuning BRCA1 and BARD1 activity to investigate RING ubiquitin ligase mechanisms. Protein science : a publication of the Protein Society 29 27977889
2016 The Association between GWAS-identified BARD1 Gene SNPs and Neuroblastoma Susceptibility in a Southern Chinese Population. International journal of medical sciences 29 26941572
2015 Functional Analysis of BARD1 Missense Variants in Homology-Directed Repair of DNA Double Strand Breaks. Human mutation 29 26350354
2012 Identification of functional SNPs in BARD1 gene and in silico analysis of damaging SNPs: based on data procured from dbSNP database. PloS one 29 23056176
2024 Germline pathogenic variants in neuroblastoma patients are enriched in BARD1 and predict worse survival. Journal of the National Cancer Institute 28 37688579
2024 Promotion of DNA end resection by BRCA1-BARD1 in homologous recombination. Nature 28 39261729
2019 Functional analysis of BARD1 missense variants in homology-directed repair and damage sensitivity. PLoS genetics 28 30925164
2015 Analysis of large mutations in BARD1 in patients with breast and/or ovarian cancer: the Polish population as an example. Scientific reports 28 25994375
2022 Metformin alleviates ionizing radiation-induced senescence by restoring BARD1-mediated DNA repair in human aortic endothelial cells. Experimental gerontology 27 35085707
2008 The BARD1 C-terminal domain structure and interactions with polyadenylation factor CstF-50. Biochemistry 27 18842000
2007 Identification of BARD1 splice-isoforms involved in human trophoblast invasion. The international journal of biochemistry & cell biology 27 17556008