Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

SET7/SET9 Antibody #2813

H3-K4-HMTase   Histone H3-K4 Methyltransferase   HMT   SET domain-containing protein 7   SET7   SET7/9   SET9   SETD7  

No. Size Price
2813S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
2813T 20 µl ( 2 western blots ) ¥1,200.00 现货查询 购买询价
2813 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 48 Rabbit
IF-IC 1:25

Species cross-reactivity is determined by western blot.

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

Specificity / Sensitivity

SET7/SET9 Antibody detects endogenous levels of total SET7/SET9 protein. This antibody does not cross-react with other SET domain-containing proteins.

SET7/SET9 Antibody能够检测内源性SET7/SET9总蛋白水平。该抗体不与其它含有SET结构域蛋白发生交叉反应。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the human SET7/SET9 protein. Antibodies are purified by protein A and peptide affinity chromatography.




Confocal immunofluorescent analysis of HeLa cells using SET7/SET9 Antibody (green). Actin filaments have been labeled with Alexa Fluor® 555 phalloidin (red).

使用SET7/SET9 Antibody (绿色),共聚焦免疫荧光分析HeLa细胞。Alexa Fluor® 555 phalloidin标记微丝蛋白(红色)。

Western Blotting

Western Blotting

Western blot analysis of cell lysates from HeLa, NIH/3T3, C6 and COS cells using SET7/SET9 Antibody.

使用SET7/SET9 Antibody,免疫印迹(Western blot)分析HeLa、NIH/3T3、C6和COS细胞中SET7/SET9的蛋白水平。


SET7/SET9 is a member of the SET domain-containing family, and can specifically methylate Lys4 on histone H3 (1). Like most other lysine-directed histone methyltransferases, it contains a conserved catalytic SET domain originally identified in the Drosophila Su(var)3-9, Enhancer of zeste and Trithorax proteins. Histone methylation is a major determinant for the formation of active and inactive regions of the genome and is crucial for the proper programming of the genome during development (2,3). Methylation of histone H3 Lys4 enhances transcriptional activation by coordinating the recruitment of BPTF, a component of the NURF chromatin remodeling complex, and WDR5, a component of multiple histone methyltransferase complexes (4,5). In addition, methylation of lysine 4 blocks transcriptional repression by inhibiting the binding of the NURD histone deacetylation complex to the amino-terminal tail of histone H3 and interfering with SUV39H1-mediated methylation of histone H3 Lys9 (1). SET7/SET9 is highly active on free histone H3, but only very weakly methylates H3 within nucleosomes (1). Besides histones, SET7/SET9 also methylates Lys189 of the TAF10, a member of the TFIID transcription factor complex, and Lys372 of the p53 tumor suppressor protein (6,7). Methylation of TAF10 stimulates transcription in a promoter-specific manner by increasing the affinity of TAF10 for RNA polymerase II, which may potentiate pre-initiation complex formation (6). Methylation of p53 at Lys372 increases protein stability and leads to upregulation of target genes such as p21. Thus the loss of SET7/SET9 may represent another mechanism for the inactivation of p53 in human cancers (7).

SET7/SET9是包含SET结构域家族的一个成员,它能特异性使histone H3蛋白Lys4位点甲基化(1)。像许多其它赖氨酸直接的组蛋白甲基转移酶一样,它包含一个保守催化的SET结构域,该结构起初被鉴定在Drosophila Su(var)3-9,、Enhancer of zeste和Trithorax蛋白中。组蛋白甲基化对于基因组的活性和非活性区域的形成起到至关重要的作用,并且在发育期间对于基因组的正确进程起着重要作用(2,3)。histone H3蛋白Lys4位点的甲基化通过协调BPTF和WDR5的招募能提高转录激活,而BPTF是NURF染色质重塑复合物的一个成分,以及WDR5是多种组蛋白甲基转移酶复合物的一个成分(4,5)。此外,通过阻止NURD组蛋白去乙酰化复合物结合到histone H3蛋白氨基端尾部以及干扰SUV39H1介导的 histone H3蛋白Lys9位点甲基化(1),lysine 4的甲基化可封闭转录抑制(1)。SET7/SET9是在游离的histone H3蛋白上的高度活性分子,但是在核小体中使H3有弱的甲基化(1)。除了组蛋白之外,SET7/SET9也可使TAF10蛋白的Lys189位点和p53肿瘤抑制蛋白的Lys372位点甲基化,而 TAF10蛋白是TFIID 转录因子复合物的成员(6,7)。以一个启动子特异性方式通过增加TAF10吸附到RAN polymerase II上,TAF10蛋白的甲基化可刺激转录(6)。p53蛋白Lys372位点的甲基化可增加蛋白质的稳定性和导致靶基因例如p21的上调。因此,在人源癌症中SET7/SET9的减少可能代表p53的失活的另外机制(7)。

  1. Nishioka, K. et al. (2002) Genes Dev. 16, 479-489.
  2. Kubicek, S. et al. (2006) Ernst Schering Res. Found. Workshop , 1-27.
  3. Lin, W. and Dent, S.Y. (2006) Curr. Opin. Genet. Dev. 16, 137-142.
  4. Wysocka, J. et al. (2006) Nature 442, 86-90.
  5. Wysocka, J. et al. (2005) Cell 121, 859-872.
  6. Kouskouti, A. et al. (2004) Mol. Cell 14, 175-182.
  7. Chuikov, S. et al. (2004) Nature 432, 353-360.

Application References

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