Product Pathways - Chromatin Regulation / Epigenetics
Brd2 (D89B4) Rabbit mAb #5848
|5848S||100 µl ( 10 western blots )||￥3,250.00||现货查询 购买询价 防伪查询|
|5848||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, ChIP=Chromatin IP, ChIP-seq=Chromatin IP-seq,
Species predicted to react based on 100% sequence homology: Rat, Monkey,
Specificity / Sensitivity
Brd2 (D89B4) Rabbit mAb recognizes endogenous levels of total Brd2 protein.
Brd2 (D89B4) Rabbit mAb兔单抗能够检测内源性Brd2总蛋白水平。
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala310 of human Brd2 protein.
Western blot analysis of extracts from MOLT-4 and NCCIT cells using Brd2 (D89B4) Rabbit mAb.
使用Brd2 (D89B4) Rabbit mAb兔单抗，免疫印迹(Western blot)分析MOLT-4和NCCIT细胞中Brd2的蛋白水平。
Chromatin immunoprecipitations were performed with cross-linked chromatin from 4 x 106 NCCIT cells and either 10 μl of Brd2 (D89B4) Rabbit mAb or 2 μl of Normal Rabbit IgG #2729 using SimpleChIP® Enzymatic Chromatin IP Kit (Magnetic Beads) #9003. The enriched DNA was quantified by real-time PCR using human GTF3C6 exon 1 primers, SimpleChIP® Human SF3B3 Exon 1 Primers #62856, and SimpleChIP® Human MyoD1 Exon 1 Primers #4490. The amount of immunoprecipitated DNA in each sample is represented as signal relative to the total amount of input chromatin, which is equivalent to one.
Chromatin immunoprecipitations were performed with cross-linked chromatin from 4 x 106 NCCIT cells and 10 μl of Brd2 (D89B4) Rabbit mAb, using SimpleChIP® Enzymatic Chromatin IP Kit (Magnetic Beads) #9005. DNA Libraries were prepared from 5 ng enriched ChIP DNA using NEBNext® Ultra™ II DNA Library Prep Kit for Illumina®, and sequenced on the Illumina NextSeq. The figure shows binding across GTF3C6, a known target gene of BRD2 (see additional figure containing ChIP-qPCR data). For additional ChIP-seq tracks, please download the product data sheet.
Brd2 is a highly conserved member of the BET subfamily of bromodomain proteins that contain two tandem N-terminal bromodomains and a single C-terminal extra-terminal (ET) domain (1). In addition to its involvement in guiding the expression of cell cycle genes through its binding to multiple E2Fs (2), Brd2 has been shown to be associated with several regulators of transcription, including TFIID and Swi/Snf complexes (3,4). First identified as a nuclear serine/threonine kinase (5), Brd2, like other bromodomain proteins, is thought to function in mammalian development by regulating chromatin structure and transcription (6). Brd2 has been shown to bind to histone H4 via acetylated Lys12, a substrate of several histone acetyltransferase transcriptional coactivators (7). In mouse, Brd2 has the highest levels of expression during embryogenesis and in the adult testis, ovaries, and brain (8,9,10). Brd2-deficient mouse embryos exhibit delayed development and eventual death due to neural tube closure defects (11). Mutations in the promoter of the Brd2 gene have been associated with increased susceptibility to juvenile myoclonic epilepsy (JME) (12).
Brd2蛋白是高度保守的溴区结构蛋白的BET亚家族成员，它包含有两个串联的N端溴区结构和一个单个的C端ET(Extra-terminal)结构域(1)。除了通过与多个E2Fs的结合能力从而涉及导向细胞周期基因的表达之外(2)，研究证明Brd2蛋白与转录的数个调节因子有关联，包含有TFIID和Swi/Snf复合物(3,4)。像其它溴区结构蛋白一样，Brd2蛋白首先被鉴定作为细胞核丝氨酸/苏氨酸激酶(5)，并且被认为通过调节染色质结构和转录从而具有在哺乳动物发育中的功能 (6)。研究证明Brd2蛋白结合到Lys12位点乙酰化的组蛋白H4上，它是数个组蛋白乙酰转移酶转录共激活因子的底物(7)。在小鼠胚胎发育以及成年睾丸、卵巢和大脑中，Brd2蛋白有最高的表达水平(8,9,10)。Brd2敲除的小鼠胚胎展示了延迟发育和最终死亡，这由于神经管关闭缺陷(neural tube closure defect,NTCD)(11)。Brd2基因启动子的突变与青少年肌阵挛性癫痫 (juvenile myoclonic epilepsy,JME)的增加的敏感性有关联(12)。
- Florence, B. and Faller, D.V. (2001) Front Biosci 6, D1008-18.
- Denis, G.V. et al. (2000) Cell Growth Differ 11, 417-24.
- Crowley, T.E. et al. (2002) Mol Endocrinol 16, 1727-37.
- Denis, G.V. et al. (2006) J Proteome Res 5, 502-11.
- Gyuris, A. et al. (2009) Biochim Biophys Acta 1789, 413-21.
- Kanno, T. et al. (2004) Mol Cell 13, 33-43.
- Shang, E. et al. (2004) Gene Expr Patterns 4, 513-9.
- Trousdale, R.K. and Wolgemuth, D.J. (2004) Mol Reprod Dev 68, 261-8.
- Pal, D.K. et al. (2003) Am J Hum Genet 73, 261-70.
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