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Brd4 associates with mitotic chromosomes throughout early zebrafish embryogenesis
Genetic and pharmacological inhibition of BRD4 suppressed IL-1beta-induced expression and translocation of HMGB1. Chromatin immunoprecipitation (ChIP) showed the enrichment of BRD4 around the HMGB1 upstream non-promoter region, which diminished with JQ1 treatment.
miR204 directly binds to UCA1 and the 3'untranslated region of BRD4. Furthermore, UCA1 competed with BRD4 for miR204 binding. miR204 knockdown enhanced BRD4 expression, which can be partially restored by short hairpinUCA1.
High BRD4 expression is associated with preeclampsia.
BRD4 silencing was negatively correlated palomid 529-induced apoptosis in the primary human renal cell carcinoma cells and tumor growth in SCID mice.
Study in melanoma cell and in vivo melanoma models provides evidence for a direct role of BRD4 binding at super-enhancers that drive the expression of PGC-1alphaalpha and SOX10, a transcription factor involved in melanocyte development.
miR-608 inhibits hepatocellular carcinoma cell proliferation possibly via targeting BET family protein BRD4.
MS645 blocks BRD4 binding to transcription enhancer/mediator proteins MED1 and YY1 with potency superior to monovalent BET inhibitors, resulting in down-regulation of proinflammatory cytokines and genes for cell-cycle control and DNA damage repair that are largely unaffected by monovalent BrD inhibition.
Study shows that BRD4 is significantly highly expressed in gastric cancer patients and cell lines and positively regulates the expression of c-MYC through transcription regulation and epigenetic levels. Functionally, these result demonstrate that the knockdown of BRD4 represses the proliferation and induces the apoptosis of gastric cancer cells through repression of c-MYC.
BRD4 hyperphosphorylation is associated with cellular transformation in NUT midline carcinoma
Results suggest structure-based drug design of bromodomain-containing protein 4 (Brd4) inhibitors.
Cells harboring the fusion gene are selectively sensitive to small-molecule inhibition of protein targets induced by, or bound to, PAX3-FOXO1-occupied super enhancers. Furthermore, PAX3-FOXO1 recruits and requires the BET bromodomain protein BRD4 to function at super enhancers, resulting in a complete dependence on BRD4 and a significant susceptibility to BRD inhibition
Our data suggested that downregulation of BRD4 in gallbladder cancer (GBC) cells induced apoptosis by PI3K/AKT pathway. Inhibition of BRD4 expression may be a novel therapeutic strategy for patients with GBC.
these results highlighted the significant genetic contribution of the ARID1B variant, rs73013281, to susceptibility for HCC, especially in interaction with physical activity.
In pluripotent cells, Brd2-Brd4 occupy Nodal gene regulatory elements (NREs), but only Brd4 is required for pluripotency gene expression. Brd4 downregulation facilitates pluripotent exit and drives enhanced Brd2 NRE occupancy, thereby unveiling a specific function for Brd2 in differentiative Nodal-Smad2 signalling
Findings reveal that PCa-associated ERG can interact and co-occupy with BRD4 in the genome, and suggest this druggable interaction is critical for ERG-mediated cell invasion and PCa progression.
Data suggest that pharmacological inhibition of BET proteins could be a potential treatment for renal fibrosis.
Our data strongly support the use of CCR2 and CD180 mRNAs as whole blood pharmacodynamic (PD)biomarkers for BRD4 inhibitors, especially in situations where paired tumor biopsies are unavailable. In addition, they can be used as tumor-based PD biomarkers for hematologic tumors.
Study identified Brd4 as a novel proline hydroxylation substrate with nearly 60% stoichiometry under normoxia states and its hydroxylation level is enzymatically regulated.
Further analysis indicated that JQ1 inhibited the recruitment of BDR4 to the promoter complex of the Myc and Ccnd1 genes in rat thyroid follicular PCCL3 cells, resulting in decreased MYC expression at the mRNA and protein levels to inhibit tumor cell proliferation
The Brd4 acetyllysine-binding protein of RelA is involved in activation of polyomavirus JC.
The protein encoded by this gene is homologous to the murine protein MCAP, which associates with chromosomes during mitosis, and to the human RING3 protein, a serine/threonine kinase. Each of these proteins contains two bromodomains, a conserved sequence motif which may be involved in chromatin targeting. This gene has been implicated as the chromosome 19 target of translocation t(15\;19)(q13\;p13.1), which defines an upper respiratory tract carcinoma in young people. Two alternatively spliced transcript variants have been described.
Bromodomain-containing protein 4B
, bromodomain-containing protein 4B
, bromodomain containing 4
, bromodomain-containing protein 4
, bromodomain 4
, bromodomain-containing protein 4-like
, bromodomain containing protein 4
, bromodomain-containing 4
, chromosome-associated protein
, bromodomain-containing 5
, fsh-like protein
, mitotic chromosome-associated protein