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Luciferase reporter assay and in vitro rescue experiment confirmed that ANRIL promoted NLRP3 inflammasome activation by up-regulating BRCC3 expression via sponging miR-122-5p.
Knockdown of BRCC3 in HeLa and SiHa cervical cancer cells revealed that BRCC3 interference inhibited the viability, in addition to the invasion and migration abilities, of cervical cancer cells via regulation of Snai family members and MMPs, which subsequently inhibit the progress of EMT.
this study shows that mitochondrial DNA oxidation induces imbalanced activity of NLRP3/NLRP6 inflammasomes by activation of caspase-8 and BRCC36 in dry eye
In late S/G2 phase, the DNA damage-responsive E3 ligase RNF8 conjugates K63-linked ubiquitin chains to tankyrase 1, while in G1 phase such ubiquitin chains are removed by BRISC, an ABRO1/BRCC36-containing deubiquitinase complex.
findings uncover a pivotal role of BRCC36 DUB in limiting DSB processing and repair and illustrate how cells may physically couple ubiquitin recognition and metabolizing activities for fine tuning of DNA repair processes.
BRCC3 may play a role in B7-H3-induced 5-Fu resistance.
BRCC3 inversely correlated with NPC overall and relapse-free survival. Its expression was higher in radioresistant NPC cells, where BRCC3 knockdown increased the cell survival fraction, attenuated DNA damage repair and resulted in G2/M cell cycle arrest.
BRCC3 likely plays a role as tumor-associated gene in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.
KIAA0157 allosterically activates a cognate deubiquitinating enzyme (DUB) partner and implicates super dimerization as a new regulatory mechanism underlying BRCC36 DUB activity.
upregulation of BRCC3 expression is associated with glioma.
these data strongly suggest that BRCC3, a deubiquitinating enzyme that is part of the cellular BRCA1 and BRISC complexes, is an important player in angiogenesis and that BRCC3 loss-of-function mutations are associated with moyamoya angiopathy.
NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes
scaffold proteins not only participate in the regulation of BRCC36 activity but also determine its subcellular localization and cellular functions.
These findings demonstrate that BRCC3 is a novel effector of Raf-1, and implicate a role of BRCC3 in modulation of p-ERK, cell survival and proliferation.
the human Ubc13/Rnf8 ubiquitin ligases control foci formation of the Rap80/Abraxas/Brca1/Brcc36 complex in response to DNA damage
Specificity for K63-linked polyubiquitin is a common property of the JAMM/MPN+ family of deubiquitinating enzymes.
The deubiquitinating enzyme, BRCC3, is a critical regulator of NLRP3 activity by promoting its deubiquitination.
This gene encodes a subunit of the BRCA1-BRCA2-containing complex (BRCC), which is an E3 ubiquitin ligase. This complex plays a role in the DNA damage response, where it is responsible for the stable accumulation of BRCA1 at DNA break sites. The component encoded by this gene can specifically cleave Lys 63-linked polyubiquitin chains, and it regulates the abundance of these polyubiquitin chains in chromatin. The loss of this gene results in abnormal angiogenesis and is associated with syndromic moyamoya, a cerebrovascular angiopathy. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 5.
BRCA1/BRCA2-containing complex, subunit 3
, BRCA1-A complex subunit BRCC36
, BRCA1/BRCA2-containing complex subunit 3
, BRCA1/BRCA2-containing complex subunit 36
, BRISC complex subunit BRCC36
, lys-63-specific deubiquitinase BRCC36
, 6.1A protein