Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

HDAC2 (3F3) Mouse mAb #5113

deacetylase   nurd complex  

No. Size Price
5113S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
5113T 20 µl ( 2 western blots ) ¥1,200.00 现货查询 购买询价 防伪查询
5113 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 60 Mouse IgG1
IP 1:50
IF-IC 1:400

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry),

Specificity / Sensitivity

HDAC2 (3F3) Mouse mAb detects endogenous levels of HDAC2 protein. The antibody does not cross-react with other HDAC proteins.

HDAC2 (3F3) Mouse mAb鼠单抗能够检测内源性HDAC2总蛋白水平。该抗体不能源其它HDAC蛋白发生交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the carboxy terminus of human HDAC2.




Confocal immunofluorescent analysis of HeLa cells using HDAC2 (3F3) Mouse mAb (green). Actin filaments were labeled using DY-554 Phalloidin (red).

使用HDAC2 (3F3) Mouse mAb鼠单抗 (绿色),共聚焦免疫荧光分析HeLa细胞。DY-554 Phalloidin标记微丝蛋白(红色)。

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using HDAC2 (3F3) Mouse mAb.

使用HDAC2 (3F3) Mouse mAb鼠单抗,免疫印迹(Western blot)分析不同细胞中HDAC2 (3F3)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).

HDAC1 and HDAC2 are highly homologous and are involved in histone deacetylation, chromatin remodeling and transcriptional repression (8-10). Both proteins are found together in numerous complexes including the nucleosome remodeling and deacetylation complex (NuRD), MeCP1, and the mSin3A corepressor complex.

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)。

HDAC1和HDAC2高度同源,都在组蛋白去乙酰化、染色质调控(chromatin remodeling)和转录抑制方面起重要作用(8-10)。这些蛋白质发现在多种蛋白复合物中,包括核小体调控和去乙酰化复合物 (NuRD),MeCP1和mSin3A共抑制复合物。

  1. Marmorstein, R. (2001) Cell Mol Life Sci 58, 693-703.
  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. Zhang, Y. et al. (1999) Genes Dev 13, 1924-35.
  9. Ng, H.H. et al. (1999) Nat Genet 23, 58-61.
  10. Zhang, Y. et al. (1997) Cell 89, 357-64.

Application References

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

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