Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

p190-A RhoGAP (D8Q6C) Rabbit mAb #12164

No. Size Price
12164S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
12164 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Hamster,Monkey, Endogenous 190 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

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

Specificity / Sensitivity

p190-A RhoGAP (D8Q6C) Rabbit mAb recognizes endogenous levels of total p190-A RhoGAP protein.

p190-A RhoGAP (D8Q6C) Rabbit mAb可以识别内源性总的p190-A RhoGAP蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn585 of human p190-A RhoGAP protein.

单克隆抗体由合成肽段免疫动物产生,该肽段与人p190-A RhoGAP蛋白的Asn585及其邻近氨基酸残基序列一致。



Immunoprecipitation of p190-A RhoGAP from Jurkat cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or p190-A RhoGAP (D8Q6C) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using p190-A RhoGAP (D8Q6C) Rabbit mAb.使用 Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2)或p190-A RhoGAP (D8Q6C) 兔mAb (lane 3)对Jurkat细胞提取物中的p190-A RhoGAP进行免疫沉淀实验。Lane1是10%上样量。使用p190-A RhoGAP (D8Q6C) Rabbit mAb进行western blot分析。

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using p190-A RhoGAP (D8Q6C) Rabbit mAb.使用p190-A RhoGAP (D8Q6C) Rabbit mAb对多种细胞提取物进行western blot分析。


Rho family GTPases are key regulators of diverse processes such as cytoskeletal organization, cell growth and differentiation, transcriptional regulation, and cell adhesion/motility. The activities of these proteins are controlled primarily through guanine nucleotide exchange factors (GEFs) that facilitate the exchange of GDP for GTP, promoting the active (GTP-bound) state, and GTPase activating proteins (GAPs) that promote GTP hydrolysis and the inactive (GDP-bound) state (1,2). 
 The p190 RhoGAP proteins are widely expressed Rho family GAPs. p190-A has been characterized as a tumor suppressor, and research studies have shown that loss or rearrangement of the chromosomal region containing the gene for p190-A is linked to tumor development (3,4). p190-A binds the mitogen-inducible transcription factor TFII-I, sequestering it in the cytoplasm and inhibiting its activity. Phosphorylation of p190-A at Tyr308 reduces its affinity for TFII-I, relieving the inhibition (5). p190-A can also inhibit growth factor-induced gliomas in mice (6) and affect cleavage furrow formation and cytokinesis in cultured cells (7). 
 Mice lacking p190-B RhoGAP show excessive Rho activation and a reduction in activation of the transcription factor CREB (8). Cells deficient in p190-B display defective adipogenesis (9). There is increasing evidence that p190 undergoes tyrosine phosphorylation, which activates its GAP domain (9-11). Levels of tyrosine phosphorylation are enhanced by Src overexpression (10,11). IGF-I treatment downregulates Rho through phosphorylation and activation of p190-B RhoGAP, thereby enhancing IGF signaling implicated in adipogenesis (9).

Rho家族GTPase是包括细胞骨架构建,细胞生长和分化,转录调控,和细胞黏附/运动等多个过程的重要调控因子。这些蛋白的活性最初时通过鸟苷酸交换因子(GEFs)控制的,帮助GDP被GTP交换,促进活性(GTP结合)状态,GTPase激活蛋白(GAPs)促进GTP纾解保持在失活(GDP-结合)状态(1,2)。 p190 RhoGAP蛋白是广泛表达的Rho家族GAPs。P190-A被认为是一种肿瘤抑制因子,研究表明染色体包含p190-A的区域缺失或者重排与癌症的发育相关(3,4)。P190-A与有丝分裂原诱导转录因子TFII-I结合,将它推入细胞质并抑制它的活性。P190-A的Tyr308磷酸化降低了它对TFII-I的亲和力,减弱抑制作用(5)。P190-A也可以小鼠的抑制生长因子-诱导的肿瘤(6)以及影响培养细胞的卵裂沟和胞质分裂(7)。 小鼠缺乏p190-B RhoGAP会表现出过度的Rho活性和转录因子CREB活性降低(8)。细胞的p190-B的缺失也会表现出脂肪形成的缺陷(9)。越来越多的证据表明p190经过酪氨酸磷酸化后会激活它的GAP结构域(9-11)。酪氨酸磷酸化的水平是通过Src过表达增强的(10,11)。IGF-I处理会磷酸化激活p190-B RhoGAP以下调Rho,随之增强脂肪形成过程中的IGF信号通路(9)。

  1. Peck, J. et al. (2002) FEBS Lett. 528, 27-34.
  2. Moon, S.Y. and Zheng, Y. (2003) Trends Cell Biol. 13, 13-22.
  3. Wang, Z. et al. (1996) Cell Growth Differ 7, 123-33.
  4. Tikoo, A. et al. (2000) Gene 257, 23-31.
  5. Jiang, W. et al. (2005) Mol Cell 17, 23-35.
  6. Wolf, R.M. et al. (2003) Genes Dev 17, 476-87.
  7. Su, L. et al. (2003) J Cell Biol 163, 571-82.
  8. Sordella, R. et al. (2002) Dev Cell 2, 553-65.
  9. Sordella, R. et al. (2003) Cell 113, 147-58.
  10. Chang, J.H. et al. (1995) J Cell Biol 130, 355-68.
  11. Roof, R.W. et al. (1998) Mol Cell Biol 18, 7052-63.

Application References

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