PREX1 (D8O8D) Rabbit mAb

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PREX1 (D8O8D) Rabbit mAb Basic information
Source Reactivity Background References
Product Name:PREX1 (D8O8D) Rabbit mAb
Synonyms:PREX1 (D8O8D) Rabbit mAb
CAS:
MF:
MW:0
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Mol File:Mol File
PREX1 (D8O8D) Rabbit mAb Structure
PREX1 (D8O8D) Rabbit mAb Chemical Properties
Safety Information
MSDS Information
PREX1 (D8O8D) Rabbit mAb Usage And Synthesis
SourceRabbit
ReactivityHuman;Monkey
BackgroundPhosphoinositide-3,4,5-triphosphateP3)-dependent Rac exchanger 1 is a Rac-specific GTP-exchange factor regulated by heterotrimeric G-protein β/γ subunits and the lipid second messenger PtdIns(3,4,5)P3. PREX1 contains two DEP domains that coordinate heterotrimeric G-protein signaling. It also contains a Dbl-homology domain, which exhibits Rac-GEF activity, and PH and PDZ domains for interacting with upstream and downstream signaling components. Originally shown to modulate cellular migration of neutrophils by Rac2 activation, it is clear that PREX1 plays a broader role in modulating cell migration. PREX1 promotes metastasis of prostate cancer and melanoma cells, affects endothelial junction integrity, and is required for platelet generation and function. Research studies suggest that PREX1 plays an essential role in mediating ErbB-dependent signaling events in breast cancer by coordinating Rac activation in response to paracrine signals within the tumor microenvironment. Activation of PREX1 downstream of ErbB3 and EGFR chemokine receptors promotes Rac activation, increased migration, proliferation, tumorigenesis, and metastasis in breast cancer cells. Consistent with this observation, deletion of PREX1 expression in mice results in resistance to melanoma metastasis. Expression of PREX1 in human tumors transplanted into mice inversely correlates with increased tumor progression and poor survival. Additional research studies suggest that PREX Rac-GEF activity is enhanced by phosphorylation in response to growth factors or hormones, and may require coincident dephosphorylation of two PH domain serine residues. The upstream kinases and precise regulatory mechanism remains elusive.
References[1] Welch, H.C. et al. (2002) Cell 108, 809-21.
[2] Hill, K. et al. (2005) J Biol Chem 280, 4166-73.
[3] Mayeenuddin, L.H. and Garrison, J.C. (2006) J Biol Chem 281, 1921-8.
[4] Barber, M.A. et al. (2007) J Biol Chem 282, 29967-76.
[5] Welch, H.C. et al. (2005) Curr Biol 15, 1867-73.
[6] Dong, X. et al. (2005) Curr Biol 15, 1874-9.
[7] Zhao, T. et al. (2007) J Leukoc Biol 81, 1127-36.
[8] Nie, B. et al. (2010) Cell Signal 22, 770-82.
[9] Qin, J. et al. (2009) Oncogene 28, 1853-63.
[10] Wong, C.Y. et al. (2011) J Biol Chem 286, 25813-22.
PREX1 (D8O8D) Rabbit mAb Preparation Products And Raw materials
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