Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

HDAC4 (4A3) Mouse mAb #5392

HD4   HD5   HD7   HD7A   HDAC4   HDAC7A   histone deacetylase   NY-CO-9  

No. Size Price
5392S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
5392T 20 µl ( 2 western blots ) ¥1,200.00 现货查询 购买询价 防伪查询
5392 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 140 Mouse IgG2a
IP 1:200

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

HDAC4 (4A3) Mouse mAb detects endogenous levels of total HDAC4 protein. The antibody does not cross-react with other HDAC proteins.

HDAC4 (4A3) Mouse mAb鼠单抗能够检测内源性HDAC4总蛋白水平。该抗体不与其它HDAC蛋白发生交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein corresponding to the amino terminus of human HDAC4 protein.


Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using HDAC4 (4A3) Mouse mAb.

使用HDAC4 (4A3) Mouse mAb鼠单抗,免疫印迹(Western blot)分析不同细胞中HDAC4 (4A3)的蛋白水平。


Acetylation of the histone tail causes chromatin to adopt an "open" conformation, allowing increased accessibility of transcription factors to DNA. The identification of histone acetyltransferases (HATs) and their large multiprotein complexes has yielded important insights into how these enzymes regulate transcription (1,2). HAT complexes interact with sequence-specific activator proteins to target specific genes. In addition to histones, HATs can acetylate nonhistone proteins, suggesting multiple roles for these enzymes (3). In contrast, histone deacetylation promotes a "closed" chromatin conformation and typically leads to repression of gene activity (4). Mammalian histone deacetylases can be divided into three classes on the basis of their similarity to various yeast deacetylases (5). Class I proteins (HDACs 1, 2, 3, and 8) are related to the yeast Rpd3-like proteins, those in class II (HDACs 4, 5, 6, 7, 9, and 10) are related to yeast Hda1-like proteins, and class III proteins are related to the yeast protein Sir2. Inhibitors of HDAC activity are now being explored as potential therapeutic cancer agents (6,7).

Histone deacetylases (HDACs) interact with an increasing number of transcription factors, including myocyte enhancer factor 2 (MEF2), to negatively regulate gene expression. HDACs are regulated in part by shuttling between the nucleus and cytoplasm, where export to the cytoplasm facilitates gene activation by removing HDACs from their target genes (8,9). The cytoplasmic export is facilitated by 14-3-3 proteins, which bind to specific phosphoserine residues on the HDAC proteins (8,9). These phosphoserine 14-3-3 binding modules are highly conserved between HDAC proteins, allowing for their collective regulation in response to specific cell stimuli. For example, the highly conserved HDAC4 Ser246, HDAC5 Ser259 and HDAC7 Ser155 residues are all phosphorylated by CAMK and PKD kinases in response to multiple cell stimuli, including VEGF-induced angiogenesis in endothelial cells, B cell and T cell activation, and differentiation of myoblasts into muscle fiber (10-14).

组蛋白尾部的乙酰化可引起染色质成为松散的构象,这允许转录因子更易接近DNA。组蛋白去乙酰化转移酶(histone acetyltransferases,HATs)的鉴定和它们的多种蛋白复合物在它们怎样酶促调节转录中已经有了重要的见解(1,2)。HAT复合物可与特异性靶基因上序列特异的激活蛋白发生相互作用。除了组蛋白之外,HATs能够使非组蛋白乙酰化,这就认为这些酶的多种功能(3)。与此相反,组蛋白去乙酰化可促进一个致密的染色质构象,并且典型地导致基因活性的抑制(4)。哺乳动物组蛋白去乙酰化酶能按照它们的类似与多种酵母去乙酰化酶划分成三类(5)。Class I蛋白 (HDACs 1、2、3和8)是与酵母Hda1样蛋白相关,并且class III蛋白是与酵母Sir2相关。目前HDAC活性的抑制剂已经被认为潜在的治疗癌症的药物(6,7)。

Histone deacetylases (HDACs)与越来越多的转录因子相互作用,包括myocyte enhancer factor 2 (MEF2),目的是负性调节基因表达。HDACs部分程度上通过在细胞核和细胞质中穿梭来被调节,在细胞质内通过从它们的靶基因上移去HDACs从而有助于基因激活(8,9)。14-3-3蛋白有助于细胞质的输出,这主要是结合到HDAC蛋白上的特异性磷酸化丝氨酸残基(8,9)。在HDAC蛋白之间这些磷酸化丝氨酸14-3-3结合模式是高度保守的,在特定的细胞刺激下这允许它们的共同调节。例如,在多种细胞刺激下高度保守的HDAC4 Ser246位点、HDAC5 Ser259位点和HDAC7 Ser155位点残基通过CAMK和PKD激酶被磷酸化,包括在内皮细胞、B细胞和T细胞激活中VEGF诱导的血管生成,以及成肌细胞分化成肌纤维(10-14)。

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  2. Gregory, P.D. et al. (2001) Exp Cell Res 265, 195-202.
  3. Liu, Y. et al. (2000) Mol Cell Biol 20, 5540-53.
  4. Cress, W.D. and Seto, E. (2000) J Cell Physiol 184, 1-16.
  5. Gray, S.G. and Ekström, T.J. (2001) Exp Cell Res 262, 75-83.
  6. Thiagalingam, S. et al. (2003) Ann. N.Y. Acad. Sci. 983, 84-100.
  7. Vigushin, D.M. and Coombes, R.C. (2004) Curr Cancer Drug Targets 4, 205-18.
  8. Grozinger, C.M. and Schreiber, S.L. (2000) Proc Natl Acad Sci USA 97, 7835-40.
  9. Wang, A.H. et al. (2000) Mol Cell Biol 20, 6904-12.
  10. Ha, C.H. et al. (2008) J Biol Chem 283, 14590-9.
  11. Wang, S. et al. (2008) Proc Natl Acad Sci USA 105, 7738-43.
  12. Matthews, S.A. et al. (2006) Mol Cell Biol 26, 1569-77.
  13. Parra, M. et al. (2005) J Biol Chem 280, 13762-70.
  14. McKinsey, T.A. et al. (2000) Nature 408, 106-11.

Application References

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Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

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