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The BRE rs7572644 and NRG3 rs1649942 genetic variants were validated in an independent cohort of EOC Portuguese patients.
C-terminal BRE might be an important contributor to this program because in a case with relapsed AML, we observed an ins(11;2) fusing CHORDC1 to BRE at the region where intragenic transcription starts in KMT2A-rearranged and KAT6A-CREBBP AML.
show that BRE facilitates deubiquitylation of CDC25A by recruiting ubiquitin-specific-processing protease 7 (USP7) in the presence of DNA damage
Results show that BRE expression is regulated by HOTTIP LncRNA. Its over-expression promotes cell proliferation and cell cycle progression inhibiting apoptosis of glioma cells.
High BRE and high EVI1 expression are mutually exclusive in MLL-AF9-positive acute myeloid leukemia patients.
High BRE expression defines a novel subtype of adult acute myeloid leukemia characterized by a favorable prognosis.
NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes
overexpression of the BRE gene is predominantly found in MLL-rearranged AML with t(9;11)(p22;q23).
A novel stress-responsive gene called BRE which interacts with TNF-receptor-1 and blocks the apoptotic effect of TNF-alpha, was identified.
These results show that BRE over-expression can indeed promote growth, though not initiation, of liver tumors.
BRE mediates antiapoptosis by inhibiting the mitochondrial apoptotic machinery
the enhanced tumor growth is more likely due to the antiapoptotic activity of BRE than any direct effect of the protein on cell proliferation
Antiapoptotic in vivo; Bre levels are regulated post-transcriptionally in the liver, which is not observed in human hepatocellular carcinoma (HCC) and non-HCC cell lines.
results implied that BRE plays a significant role in mediating antiapoptotic and proliferative responses in esophageal carcinoma cells
Bre enhances osteoblastic differentiation by promoting the Mdm2-mediated degradation of p53.
results demonstrate a role for BRE in both replicative senescence and DNA damage-induced premature senescence. This can be attributed to BRE being required for BRCA1-A complex-driven HR DNA repair
Depletion of BRE also increased tumor cell apoptosis, and decreased both local and metastatic tumor growth.
a highly conserved gene in two species can generate alternative transcripts different in both of the sequence structure and expression pattern, as well as a similar class of transcripts resulting from unconventional transcript processing.
BRE has a role in the regulation of key proteins of the cellular stress-response machinery, including prohibitin and p53
Component of the BRCA1-A complex, a complex that specifically recognizes 'Lys-63'-linked ubiquitinated histones H2A and H2AX at DNA lesions sites, leading to target the BRCA1-BARD1 heterodimer to sites of DNA damage at double-strand breaks (DSBs). The BRCA1-A complex also possesses deubiquitinase activity that specifically removes 'Lys-63'-linked ubiquitin on histones H2A and H2AX. In the BRCA1-A complex, it acts as an adapter that bridges the interaction between BABAM1/NBA1 and the rest of the complex, thereby being required for the complex integrity and modulating the E3 ubiquitin ligase activity of the BRCA1-BARD1 heterodimer. Probably also plays a role as a component of the BRISC complex, a multiprotein complex that specifically cleaves 'Lys-63'-linked ubiquitin (By similarity).
BRCA1-A complex subunit BRE
, BRCA1/BRCA2-containing complex subunit 45
, Brain and reproductive organ-expressed protein
, brain and reproductive organ-expressed (TNFRSF1A modulator)
, BRCA1-A complex subunit BRE-like
, BRCA1/BRCA2-containing complex, subunit 4
, brain and reproductive organ-expressed protein