Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

Phospho-eNOS (Ser113) Antibody #9575

EC-NOS   Endothelial NOS   nitric oxide   NOS-111  

No. Size Price
9575S 100 µl ( 10 western blots ) ¥4,050.00 现货查询 购买询价 防伪查询
9575 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Bovine, Endogenous 140 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

Phospho-eNOS (Ser113) Antibody detects endogenous levels of eNOS only when phosphorylated at serine 113.

Phospho-eNOS (Ser113) Antibody仅检测Ser113位点磷酸化的内源性总eNOS蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser113 of human eNOS. Antibodies are purified by protein A and peptide affinity chromatography.


Western Blotting

Western Blotting

Western blot analysis of extracts from bovine aoric endothelial cells (BAEC), untreated or treated with lamda phosphatase, using Phospho-eNOS (Ser113) Antibody (upper) or eNOS antibody (lower).

Western blot分析牛动脉内皮细胞(BAEC),未处理组和λ磷酸酶处理组,所用抗体为Phospho-eNOS (Ser113) Antibody (上) 或eNOS antibody (下).


Endothelial nitric-oxide synthase (eNOS) is an important enzyme in the cardiovascular system. It catalyzes the production of nitric oxide (NO), a key regulator of blood pressure, vascular remodeling, and angiogenesis (1,2). The activity of eNOS is regulated by phosphorylation at multiple sites. The two most thoroughly studied sites are the activation site Ser1177 and the inhibitory site Thr495 (3). Several protein kinases including Akt/PKB, PKA, and AMPK activate eNOS by phosphorylating Ser1177 in response to various stimuli (4,5). In contrast, bradykinin and H2O2 activate eNOS activity by promoting both Ser1177 phosphorylation and Thr495 dephosphorylation (6,7).eNOS is activated by VEGF, and this activation is associated with dephsophorylation of eNOS at serine 113. Cyclosporin A blocks this dephosphorylation of eNOS upon VEGF stimulation (8).

内皮一氧化氮合酶(eNOS)是心血管系统的一种重要的酶。它可以催化合成一氧化氮(NO)。NO是一种血压,血管重建和生成的重要的调节因子(1,2)。eNOS的活性受多个位点磷酸化的调控。研究最为透彻的两个位点是激活位点Ser1177 和抑制位点Thr495(3)。几种蛋白激酶包括Akt/PKB, PKA 和AMPK都可以在不同的刺激下通过 Ser1177位点的磷酸化来激活eNOS的活性(4,5)。相反,血管舒缓激肽和过氧化氢通过促进Ser1177的磷酸化和Thr495的去磷酸化来激活eNOS的活性(6,7)。eNOS可以被VEGF激活,并与Ser113位点eNOS的去磷酸化有关。细胞色素A通过VEGF刺激调节来阻断eNOS的去磷酸化(8)。

  1. Fulton, D. et al. (2001) J Pharmacol Exp Ther 299, 818-24.
  2. Shaul, P.W. (2002) Annu Rev Physiol 64, 749-74.
  3. Chen, Z.P. et al. (1999) FEBS Lett 443, 285-9.
  4. Dimmeler, S. et al. (1999) Nature 399, 601-5.
  5. Fulton, D. et al. (1999) Nature 399, 597-601.
  6. Harris, M.B. et al. (2001) J Biol Chem 276, 16587-91.
  7. Thomas, S.R. et al. (2002) J Biol Chem 277, 6017-24.
  8. Kou, R. et al. (2002) J Biol. Chem. 277(33) , 29669-29673.

Application References

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