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BRD7 encodes a protein which is a member of the bromodomain-containing protein family. Additionally we are shipping BRD7 Antibodies (66) and BRD7 Kits (2) and many more products for this protein.
Showing 6 out of 6 products:
the transcriptional signature of low BRD7 expressing cells is associated with increased angiogenesis.
our data indicated that BRD7 may serve as a tumor suppressor in hepatocellular carcinoma
Results demonstrate a novel function of BRD7 in TGF-beta (show TGFB1 Proteins) signaling. BRD7 interacts with the Smad (show SMAD1 Proteins) tumor suppressor complex, and enhances both DNA-binding ability and transcriptional activity of Smads. BRD7 functions in growth inhibition and tumor suppression partly as a transcriptional co-activator of Smads.
Overexpression of BRD7 inhibited cyclin D and myc (show MYC Proteins) expression. Our findings are consistent with a tumor suppressor role for BRD7 in lung adenocarcinoma tumorigenesis.
the expression of miR (show MLXIP Proteins)-141 in BRD7-overexpressing NPC (show NPC1 Proteins) cells could partially reverse the tumor suppressive effect of BRD7 on cell proliferation and tumor growth in vitro and in vivo.
constructed a regulating network of BRD7 downstream genes, and this network suggests multiple feedback regulations of the pathways. Furthermore, we validated BIRC2 (show BIRC2 Proteins), BIRC3 (show BIRC3 Proteins), TXN2 (show TXN2 Proteins), and NOTCH1 (show NOTCH1 Proteins) genes as direct, functional BRD7 targets
Propose that the balance between BRD7 function and Ras/Raf (show RAF1 Proteins)/MEK (show MAP2K1 Proteins)/ERK (show EPHB2 Proteins) activity is important for determining the outcomes of HCV infection and HCC (show FAM126A Proteins) development.
Ectopic expression of BRD7 could significantly inhibit miR (show MLXIP Proteins)-300-promoted proliferation, invasion and epithelial-mesenchymal transition in osteosarcoma.
BRD7 promoter hypermethylation is an indicator of well differentiated oral squamous cell carcinomas.
Data indicate that bromodomain-containing protein 7 (BRD7) was a direct target of microRNA-410 (miR (show MLXIP Proteins)-410).
these findings suggest that BRD7 has an anti-inflammatory role during early acute inflammation by inhibiting activation of the NF-small ka, CyrillicB signaling pathway, which provides evidence to aid in understanding the therapeutic effects of BRD7 on inflammatory diseases
Furthermore, Brd7 inhibition alters the phenotype of macrophages and promotes plaque instability, at least partly via STAT6 (show STAT6 Proteins) signaling. Our data define a previously undescribed role of Brd7 in the development of atherosclerosis.
Homozygous BRD7 knockout (KO) mice showed retardation in development.
Homozygous knockout of BRD7 (BRD7(-/-)) resulted in complete male infertility and spermatogenesis defects, including deformed acrosomal formation, degenerative elongating spermatids and irregular head morphology in postmeiotic germ cells in the seminiferous epithelium, which led to the complete arrest of spermatogenesis at step 13.
Results link BRD7 to medial prefrontal cortex synaptic plasticity regulation; knockout leads to impaired cognitive behavior accompanied by reduced synaptic related proteins expression and dendritic spines or branching in the medial prefrontal cortex
BRD7 interacts with the regulatory subunits of phosphatidylinositol 3-kinase (PI3K) and increases the nuclear translocation of both p85alpha and p85beta and the spliced form of XBP1 (show XBP1 Proteins) (XBP1s).
TRIM24 (show TRIM24 Proteins) regulates AR-mediated transcription in collaboration with TIP60 (show KAT5 Proteins) and BRD7.
BRD7 is a novel PBAF-specific SWI (show SMARCA1 Proteins)/SNF (show SNRPA Proteins) subunit that is required for target gene activation and repression in embryonic stem cells
This gene encodes a protein which is a member of the bromodomain-containing protein family. The product of this gene has been identified as a component of one form of the SWI/SNF chromatin remodeling complex, and as a protein which interacts with p53 and is required for p53-dependent oncogene-induced senescence which prevents tumor growth. Pseudogenes have been described on chromosomes 2, 3, 6, 13 and 14. Alternative splicing results in multiple transcript variants.
bromodomain containing 7
, nuclear transcriptor-like protein
, bromodomain-containing protein 7-like
, bromodomain-containing protein 7
, 75 kDa bromodomain protein
, protein CELTIX-1
, bromodomain protein 75 kDa
, bromodomain-containing 7
, protein tyrosine phosphatase, non-receptor type 13 interacting protein