BRD7 Antibody (Rabbit mAb) [N9J16]

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IHC1:200

Application
WB, IP, IHC, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
74 kDa

Positive Control	Prostate carcinoma; Human testis; RKO cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
BRD7 Antibody (Rabbit mAb) [N9J16] detects endogenous levels of total BRD7 protein.

Clone
N9J16

Synonym(s)
Rabbit Recombinant Monoclonal BRD7 antibody. Suitable for Flow Cyt, ICC, IHC-P, IP, WB and reacts with Human samples. Immunogen corresponding to Synthetic Peptide within Human BRD7 aa 600-700.

Background
BRD7 belongs to the bromodomain-containing protein family and functions as a core subunit of the PBAF form of the SWI/SNF chromatin remodeling complex, contributing to nucleosome remodeling at target gene promoters through this larger multiprotein assembly. BRD7 operates as a dual transcriptional regulator, acting as a coactivator at certain promoters and a corepressor at others depending on the associated complex and target gene context. As a p53 coactivator, BRD7 interacts directly with the acetyltransferase p300 and stimulates acetylation of both p53 and local histones at target promoters, and this interaction is specifically required for p53-mediated transcriptional activation and permanent cell-cycle arrest following oncogene-induced stress signaling. Loss of BRD7 impairs oncogene-induced senescence despite normal p53 protein levels, indicating that BRD7 acts downstream of p53 stabilization at the level of promoter-specific transcriptional output rather than controlling p53 abundance. Independent of the p53 axis, BRD7 binds directly to BRCA1 as part of the SWI/SNF complex and regulates BRCA1-dependent transcription, including recruitment of BRCA1 and POU2F1 to the ESR1 promoter, where BRD7 binding increases histone H3 lysine-9 acetylation and modulates estrogen receptor-alpha expression. BRD7 additionally activates Wnt signaling in a DVL1-dependent manner by suppressing GSK3B phosphotransferase activity and promoting GSK3B dephosphorylation, linking chromatin-level regulation to a parallel cytoplasmic signaling pathway. BRD7 inhibits progression from G1 into S phase, restraining proliferation through this cell-cycle checkpoint function. Reduced BRD7 expression has been identified in nasopharyngeal carcinoma and breast cancer, where loss of BRD7-mediated p53 and BRCA1 pathway engagement is associated with impaired tumor-suppressive transcriptional programs, positioning BRD7 as a chromatin-associated cofactor whose activity connects SWI/SNF remodeling to both p53- and BRCA1-dependent gene regulation in these cancer contexts.

Background

BRD7 belongs to the bromodomain-containing protein family and functions as a core subunit of the PBAF form of the SWI/SNF chromatin remodeling complex, contributing to nucleosome remodeling at target gene promoters through this larger multiprotein assembly. BRD7 operates as a dual transcriptional regulator, acting as a coactivator at certain promoters and a corepressor at others depending on the associated complex and target gene context. As a p53 coactivator, BRD7 interacts directly with the acetyltransferase p300 and stimulates acetylation of both p53 and local histones at target promoters, and this interaction is specifically required for p53-mediated transcriptional activation and permanent cell-cycle arrest following oncogene-induced stress signaling. Loss of BRD7 impairs oncogene-induced senescence despite normal p53 protein levels, indicating that BRD7 acts downstream of p53 stabilization at the level of promoter-specific transcriptional output rather than controlling p53 abundance. Independent of the p53 axis, BRD7 binds directly to BRCA1 as part of the SWI/SNF complex and regulates BRCA1-dependent transcription, including recruitment of BRCA1 and POU2F1 to the ESR1 promoter, where BRD7 binding increases histone H3 lysine-9 acetylation and modulates estrogen receptor-alpha expression. BRD7 additionally activates Wnt signaling in a DVL1-dependent manner by suppressing GSK3B phosphotransferase activity and promoting GSK3B dephosphorylation, linking chromatin-level regulation to a parallel cytoplasmic signaling pathway. BRD7 inhibits progression from G1 into S phase, restraining proliferation through this cell-cycle checkpoint function. Reduced BRD7 expression has been identified in nasopharyngeal carcinoma and breast cancer, where loss of BRD7-mediated p53 and BRCA1 pathway engagement is associated with impaired tumor-suppressive transcriptional programs, positioning BRD7 as a chromatin-associated cofactor whose activity connects SWI/SNF remodeling to both p53- and BRCA1-dependent gene regulation in these cancer contexts.

References
https://pubmed.ncbi.nlm.nih.gov/20215511/ https://pubmed.ncbi.nlm.nih.gov/20228809/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%