Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human BRD4 Anticorps:
anti-Mouse (Murine) BRD4 Anticorps:
anti-Rat (Rattus) BRD4 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal BRD4 Primary Antibody pour ICC, IF - ABIN438710
Rahman, Sowa, Ottinger, Smith, Shi, Harper, Howley: The Brd4 extraterminal domain confers transcription activation independent of pTEFb by recruiting multiple proteins, including NSD3. dans Molecular and cellular biology 2011
Show all 3 Pubmed References
Human Polyclonal BRD4 Primary Antibody pour ICC, IF - ABIN4285227
Zuber, Shi, Wang, Rappaport, Herrmann, Sison, Magoon, Qi, Blatt, Wunderlich, Taylor, Johns, Chicas, Mulloy, Kogan, Brown, Valent, Bradner, Lowe, Vakoc: RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia. dans Nature 2011
Show all 2 Pubmed References
Human Polyclonal BRD4 Primary Antibody pour ChIP, WB - ABIN2668492
Flajollet, Rachez, Ploton, Schulz, Gallais, Métivier, Pawlak, Leray, Issulahi, Héliot, Staels, Salbert, Lefebvre: The elongation complex components BRD4 and MLLT3/AF9 are transcriptional coactivators of nuclear retinoid receptors. dans PLoS ONE 2013
Show all 2 Pubmed References
Brd4 associates with mitotic chromosomes throughout early zebrafish embryogenesis
Pancreatic stellate cells (PSCs), the predominant fibroblasts in human pancreatic ductal adenocarcinoma tumors, express high levels of PD-L1 and the interplay between IRF1 and BRD4 regulates PD-L1 expression in PSCs.
we describe the dependency of EWS/ETS-driven transcription upon chromatin reader BET bromdomain proteins and investigate the potential of BET inhibitors in treating EWS. EWS/FLI1 and EWS/ERG were found in a transcriptional complex with BRD4, and knockdown of BRD2/3/4 significantly impaired the oncogenic phenotype of EWS cells. RNA-seq analysis following BRD4 knockdown or inhibition with JQ1 revealed an attenuated EWS/ETS
Combined inhibition of HDAC1/2 and Brd4 resolved the aberrant ISG expression detected in cells derived from patients with two inherited interferonopathies, ISG15 and USP18 deficiencies, defining a novel therapeutic approach to ISG-associated autoimmune diseases.
a BRD4/miR-216a-3p/Wnt/beta-catenin pathway in regulating the stemness of gastric cancer cells
The BRD4-KDM5C-PTEN may be a new oncogenic pathway in CRPC development.
the importance of BRD4/B7-H3/TLR4 pathway
results suggest a mechanism by which eRNAs are directly involved in gene regulation by modulating enhancer interactions and transcriptional functions of BRD4
The above anticancer effects was associated with the downregulation of BRD4.
Results provide evidence that both BRD3 and BRD4 are repressors of epithelial-to-mesenchymal transition in breast cancer cells.
the synergistic effect is likely due to two reasons: (i) Plk1 inhibition results in the accumulation of beta-catenin in the nucleus, thus elevation of c-MYC expression, whereas JQ1 treatment directly suppresses c-MYC transcription; (ii) Plk1 and BRD4 dual inhibition acts synergistically in inhibition of AR signaling.
Authors demonstrate a novel role for BRD4 in the formation of oncogenic TMPRSS2-ERG fusions via its involvement in the NHEJ DNA repair pathway.
Recruitment of Brd4 (and Brd3) is essential for the inflammation mediator-induced matrix-degrading enzyme expression.
The direct relationship between bromodomain containing 4 (BRD4) and breast cancer 1, early onset protein (BRCA1)/Rad51 Recombinase (RAD51) expression was confirmed in triple negative breast cancer (TNBC) cells.
PES1 is transcriptionally regulated by BRD4 and promotes cell proliferation and glycolysis in hepatocellular carcinoma
findings suggest that resistance to I-BET151 in U937R cells is related to constitutive activation of the NF-kappaB signaling pathway via increased expression of both BRD2 and BRD4. Targeting the NF-kappaB signaling pathway may be an effective therapeutic strategy to enhance or restore the sensitivity to I-BET151 in U937 cells.
High BRD4 expression is associated with Pancreatic ductal adenocarcinoma.
BRD4 and NIPBL displayed correlated binding at super-enhancers and appeared to co-regulate developmental gene expression.
Ectopic SPZ1 and TWIST1 expression, but not that of TWIST1 alone, enhanced VEGF expression via the recruitment of BRD4, enhancing RNA-Pol II-dependent transcription and inducing metastasis. Acetylation signaling functions in the SPZ1-TWIST1-BRD4 axis in the mediation of EMT and its regulation during tumor initiation and metastasis
This work sheds light on essential mediators, mechanisms and genome-wide regulatory elements that are responsible for transcriptional addiction in cancer and lays the groundwork for a rational use of BET inhibitors according to YAP/TAZ biology.
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.
Time-series modeling of cerebellar granule cell progenitors (GCP) cell cycle exit identified downregulation of activity of the epigenetic reader protein Brd4. Brd4 binding to the Gli1 locus is controlled by casein kinase 1delta-dependent phosphorylation during GCP proliferation and decreases during GCP cell cycle exit.
RelA-BRD4 signaling in distal tracheobronchiolar epithelial cells mediates acute inflammation in response to luminal viral patterns.
These findings indicate that BRD4 regulates the Adipoq gene by recruiting P-TEFb onto acetylated histones in the transcribed region of the gene and regulates adipocyte differentiation by regulating the expression of genes related to insulin sensitivity.
miR-29a negatively regulates hepatic stellate cell activation by inhibiting BRD4 and EZH2 function.
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.
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.
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 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