Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Expression of human BRE in multiple isoforms.
Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair.
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BRCC45 enhances BRCA1/BARD1 E3 activity and is needed for IR resistance.
"Reconstitution of a recombinant four-subunit complex containing BRCA1/BARD1/BRCC45/BRCC36 revealed an enhanced E3 ligase activity compared to that of BRCA1/BARD1 heterodimer."
A death receptor-associated anti-apoptotic protein, BRE, inhibits mitochondrial apoptotic pathway.
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BRE binds TNF-R1 and Fas and is anti-apoptotic.
"Here we show that BRE also binds to another death receptor, Fas, and upon overexpression conferred resistance to apoptosis induced by TNF-alpha, anti-Fas agonist antibody, cycloheximide, and a variety of stress-related stimuli."
Towards a proteome-scale map of the human protein-protein interaction network.
RAP80 targets BRCA1 to specific ubiquitin structures at DNA damage sites.
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RAP80 targets the BRCA1-BARD1/BRCC36 complex to K63/K6 chains at DSBs.
"RAP80 targets a complex containing the BRCA1-BARD1 (BRCA1-associated ring domain protein 1) E3 ligase and the deubiquitinating enzyme (DUB) BRCC36 to MDC1-gammaH2AX-dependent lysine(6)- and lysine(63)-linked ubiquitin polymers at DSBs."
K63-specific deubiquitination by two JAMM/MPN+ complexes: BRISC-associated Brcc36 and proteasomal Poh1.
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BRISC is a K63-specific DUB complex.
"When we analysed the individual complexes, we found that the activity was intrinsic to PA700 and the Brcc36 isopeptidase complex (BRISC), but that the CSN-associated activity was due entirely to an interaction with Brcc36."
MERIT40 controls BRCA1-Rap80 complex integrity and recruitment to DNA double-strand breaks.
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MERIT40 is essential for BRCA1-Rap80 complex integrity.
"Here, we identify MERIT40 (Mediator of Rap80 Interactions and Targeting 40 kD)/(C19orf62) as a Rap80-associated protein that is essential for BRCA1-Rap80 complex protein interactions, stability, and DSB targeting."
MERIT40 facilitates BRCA1 localization and DNA damage repair.
NBA1, a new player in the Brca1 A complex, is required for DNA damage resistance and checkpoint control.
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Four BRCA1-A members bind polyubiquitin chains.
"Furthermore, we show that four members of the BRCA1-A complex possess a polyubiquitin chain-binding capability, thus forming a complex that might facilitate the deubiquitinating activity of the deubiquitination enzyme BRCC36 or the E3 ligase activity of the BRCA1/BARD1 ligase."
Defining the human deubiquitinating enzyme interaction landscape.
Differential regulation of JAMM domain deubiquitinating enzyme activity within the RAP80 complex.
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Abraxas and BRCC45 are needed for BRCC36 DUB activity.
"Abraxas and BRCC45 were essential for BRCC36 DUB activity within the RAP80 complex, whereas KIAA0157/Abro was the only interaction required for DUB activity within the BRISC."
BRCA1 tumor suppressor network: focusing on its tail.
A BRISC-SHMT complex deubiquitinates IFNAR1 and regulates interferon responses.
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BRISC-SHMT2 deubiquitinates IFNAR1.
"BRISC-SHMT2 complexes localize to and deubiquitinate actively engaged IFNAR1, thus limiting its K63-Ub-mediated internalization and lysosomal degradation."
Architecture of the human interactome defines protein communities and disease networks.
Metabolic control of BRISC-SHMT2 assembly regulates immune signalling.
Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation.
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BRE is a core BRISC/BRCA1-A component.
"BRCA1-A and BRISC also contain proteins MERIT40 (Feng et al., 2009, Shao et al., 2009, Wang et al., 2009) and BRE (Feng et al., 2009, Hu et al., 2011a) as core components."
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
AI-guided pipeline for protein-protein interaction drug discovery identifies a SARS-CoV-2 inhibitor.
Identification of a brain- and reproductive-organs-specific gene responsive to DNA damage and retinoic acid.
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BRE mRNA falls after UV and 4NQO.
"Treatment of fibroblast cell with UV and 4-nitroquinoline-1-oxide caused more than 90% and 50% decreases in BRE mRNA, respectively."
BRE: a modulator of TNF-alpha action.
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Y2H found TNF-R1 but not Fas binding.
"In the yeast two-hybrid assay, BRE specifically interacted with p55 TNF receptor but not with other TNF family members such as the Fas receptor, the p75 TNF receptor, and p75 neurotrophin receptor."
Formation of BRCA1-A complex at DNA DSBs
CHEK2 is recruited to DNA DSBs
CHEK2 phosphorylates BRCA1
RIF1 and PAX1IP bind TP53BP1 at DNA DSBs
BRCA1-A complex deubiquitinates K63polyUb-histone H2A
BRISC complex deubiquitinates NLRP3
Phosphorylation of BRCA1-A complex at multiple sites by ATM
Phosphorylation and activation of CHEK2 by ATM
UniProt entry Q9NXR7 (BABA2_HUMAN)
Affinage mechanistic annotation for BABAM2 (human)
NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes.
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NBA1-BRE interaction maintains both complexes.
"Here, we found that the two complexes are assembled in a similar manner and NBA1 and BRE interaction is critical for maintaining the integrity of both of the complexes."
BRE/BRCC45 regulates CDC25A stability by recruiting USP7 in response to DNA damage.
BRE plays an essential role in preventing replicative and DNA damage-induced premature senescence.
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BRE-null fibroblasts keep gamma-H2AX foci longer after IR.
"We also demonstrated that the gamma irradiation induced γ-H2AX foci, a DNA damage marker, persisted significantly longer in BRE(-/-) fibroblasts than in WT fibroblasts, confirming that the DNA repair process is impaired in the absence of BRE."
Anti-apoptotic protein BRE/BRCC45 attenuates apoptosis through maintaining the expression of caspase inhibitor XIAP in mouse Lewis lung carcinoma D122 cells.
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BRE maintains XIAP levels in a mouse carcinoma line.
"Here we report based on the use of a mouse Lewis lung carcinoma cell line D122 that BRE has an essential role in maintaining the cellular protein level of XIAP, which is the most potent endogenous inhibitor of the caspases functioning in both extrinsic and intrinsic apoptosis."