BRD2 Antibody (YA3910)
(Synonyms: FSH; NAT; RNF3; FSRG1; RING3; D6S113E; O27.1.1)BRD2 Antibody (YA3910) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to BRD2.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, FC, ELISA
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Reactivity :
Human, Rat
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Formulation:
Supplied in PBS with 0.05% sodium azide
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:400 | 1:10000 |
Product Details
BRD2 Antibody (YA3910) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to BRD2.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Rat
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Observed Molecular WeightObserved band size: 110 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 88 kDa
Purified recombinant fragment of human BRD2 (AA: 227-364) expressed in E. Coli.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% sodium azide
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
BRD2 is a BET-family epigenetic reader with tandem bromodomains that bind lysine-acetylated histones and transcription factors, recruit transcription factors and coactivators, and support RNA polymerase II-dependent transcriptional elongation[1]. Mechanistically, BET proteins including BRD2, BRD3, BRD4, and BRDT connect acetylated chromatin to gene-expression programs that regulate transcription, chromatin remodeling, DNA replication, and DNA damage repair[1]. In pancreatic β-cells, BET inhibition with JQ1 increased insulin secretion and insulin content, while specific inhibition of Brd2 increased fatty acid oxidation, showing a discrete metabolic role for BRD2 compared with other BET isoforms[2]. Compared with BRD4, BRD2 appears less dominant in several disease models: BRD4, not BRD2 or BRD3, increased after repeated cocaine exposure, and BRD4 was preferentially linked to cocaine-induced Bdnf expression[3]. In prostate cancer, BET proteins BRD2, BRD3, and BRD4 are stabilized by SPOP mutations, contributing to BET-inhibitor resistance, but BRD4 often carries the main disease-specific transcriptional signal[4]. For experimental applications, pan-BET inhibitors such as JQ1, I-BET, OTX015, and RVX-208 help probe BRD2-containing acetyl-lysine reader complexes, although their limited isoform selectivity requires paired genetic approaches for BRD2-specific interpretation[5].
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Subcellular Localization
Nucleus; Chromosome
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Isoforms & Post-Translational Modification
P25440 has 4 isomers: P25440-1: 88061 Da (predicted); P25440-2: 92033 Da (predicted); P25440-3: 83151 Da (predicted); P25440-4: 74881 Da (predicted).
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Subunit
Homodimer (PubMed:17148447, PubMed:17848202, PubMed:20048151, PubMed:20709061). Interacts with E2F1 (PubMed:17148447). Interacts with (acetylated) STAT3; promoting STAT3 recruitment to chromatin (PubMed:28262505). Interacts with CTCF; promoting BRD2 recruitment to chromatin (By similarity)
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SwissProt ID
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Synonyms
FSH; NAT; RNF3; FSRG1; RING3; D6S113E; O27.1.1
Documentation
[1]. Cheung KL, et al. The Functions of BET Proteins in Gene Transcription of Biology and Diseases. Front Mol Biosci. 2021 Sep 3;8:728777. [Content Brief]
[2]. Deeney JT, et al. BET Bromodomain Proteins Brd2, Brd3 and Brd4 Selectively Regulate Metabolic Pathways in the Pancreatic β-Cell. PLoS One. 2016 Mar 23;11(3):e0151329. [Content Brief]
[3]. Sartor GC, et al. Epigenetic Readers of Lysine Acetylation Regulate Cocaine-Induced Plasticity. J Neurosci. 2015 Nov 11;35(45):15062-72. [Content Brief]
[4]. Dai X, et al. Prostate cancer-associated SPOP mutations confer resistance to BET inhibitors through stabilization of BRD4. Nat Med. 2017 Sep;23(9):1063-1071. [Content Brief]
[5]. Lucas X, et al. Targeting the BET family for the treatment of leukemia. Epigenomics. 2014 Apr;6(2):153-5. [Content Brief]
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