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Brd4 associates with mitotic chromosomes throughout early zebrafish embryogenesis
BRD4 and PML/RARalpha co-existed on the same regulatory regions of their target genes. Hence, the study showed a new discovery of the interaction of BRD4 and PML/RARalpha, as well as the decline of PML/RARalpha expression in NB4 cells, under JQ1 treatment.
DUB3 promotes BET inhibitor resistance and cancer progression by deubiquitinating BRD4.
Study suggested that the aberrant expression of BRD4 in prostate cancer may induce carcinogenesis. In addition, a mechanism by which BRD4 inhibition suppresses cell proliferation via the regulation of FOXO1-p21-Myc signaling was proposed.
A new biological function of BRD4.
SRPK1 inhibition produces a significant switch from the short to the long BRD4 isoform at the mRNA and protein levels.
Tumoral BRD4 expression in breast cancer is significantly associated with T-bet+ TILs, clinicopathological features, and a poor disease-free survival in the absence of T-bet+ TILs.
Acetylated FOXO3a recognizes the BD2 domain of BRD4, recruits the BRD4/RNAPII complex to the CDK6 gene promoter, and induces its transcription.
BRD4 amplification in cancer has oncogenic potential; BRD4-amplified High-grade Serous Ovarian Cancer is a potential patient population that could benefit from BET inhibitors
Direct interactions between AIRE, NF-kappaB, and P-TEFb result in efficient transcription of their target genes.
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
Pluripotency transcription factors and Tet1/2 maintain Brd4-independent stem cell identity in mouse embryonic stem cells.
Results provide evidence that BRD4 is required for myogenic differentiation through its preferential binding to the Myog promoter during C2C12 myoblast differentiation.
Brd4 deletion prevents enhancer RNA production, cell identity gene induction and cell differentiation. Interestingly, Brd4 is dispensable for maintaining cell identity genes in differentiated cells. These findings identify Brd4 as an enhancer epigenomic reader that links active enhancers with cell identity gene induction in differentiation.
results suggest that rhythmic expression of Sglt1 is regulated at the mRNA transcriptional elongation level by enhancing the binding of the BRD4-P-TEFb complex to acetylated histones at the gene upon BMAL1-CLOCK binding to Sglt1
Bromodomain protein BRD4 promotes cell proliferation in skin squamous cell carcinoma.
By modulating the translation of IkappaBalpha via the Mnk2-eIF4E pathway, Brd4 provides an additional layer of control for NF-kappaB-dependent inflammatory gene expression and inflammatory response.
Using compound selectivity engineering and CRISPR/Cas9 genome editing, distinct functions for Erk5 and Brd4 in pluripotency regulation of mouse embryonic stem cells have been revealed.
Long-term treatment with bromodomain-containing protein 4 (BRD4) inhibitors caused telomere shortening in both mouse and human cells, suggesting BRD4 plays a role in telomere maintenance in vivo.
Fmr1 knockout (KO) mice show widespread changes in histone marks as well as transcriptional misregulation resulting in increased expression of many critical synaptic genes. Data suggest that one chromatin target of FMRP, the reader protein Brd4, appears to be significantly involved in this transcriptional disruption.
The functional domains of mouse BRD4 and its role in transcription are described. Review.
Brd2 and Brd4 genetic transcription required for Th17 cell development and adaptive immunity.
These data provide a detailed mechanism for how activated NF-kappaB and BRD4 control epithelial-mesenchymal transition initiation and transcriptional elongation in model airway epithelial cells in vitro and in a murine pulmonary fibrosis model in vivo.
DOT1L, via dimethylated histone H3 K79, facilitates histone H4 acetylation, which in turn regulates the binding of BRD4 to chromatin in acute lymphoblastic leukemia.
Acute induction of genes related to lipid accumulation in the livers of mice force-fed with fructose is associated with the induction of histone acetylation and BRD4 binding around these genes
Both mouse and human BRD4 have intrinsic histone acetyltransferase activity.
the interaction between BRD4 and Mediator has functional importance for gene-specific transcriptional activation and for acute myeloid leukemia maintenance.
our data demonstrate the fundamental role of Brd4 in monitoring cell differentiation through its interaction with acetylated histone marks and disruption of Brd4 may cause aberrant differentiation.
Data show that CCAAT-enhancer-binding protein-alpha (C/EBPalpha) directly regulates Kruppel-like factor 4 (Klf4) expression and increasing the levels of histone demethylase Lsd1 and transcription factor Brd4 in B cell.
BRD4 can act as a global genomic regulator to direct the fibrotic response through its coordinated regulation of myofibroblast transcription.
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