|Application ||WB, IHC, IF|
|Calculated MW||116403 Da|
|Other Names||Ras GTPase-activating protein 1, GAP, GTPase-activating protein, RasGAP, Ras p21 protein activator, p120GAP, RASA1, GAP, RASA|
|Target/Specificity||A synthetic peptide corresponding to residues near the SH3 domain of human RasGAP was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||RasGap Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Inhibitory regulator of the Ras-cyclic AMP pathway. Stimulates the GTPase of normal but not oncogenic Ras p21; this stimulation may be further increased in the presence of NCK1.|
|Tissue Location||In placental villi, detected only in the trophoblast layer (cytotrophoblast and syncytiotrophoblast). Not detected in stromal, endothelial or Hofbauer cells (at protein level).|
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Provided below are standard protocols that you may find useful for product applications.
RasGAP, a regulator of Ras and Rho, stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. RasGAP is a Caspase 3 substrate (1) and acts as both pro- and anti-apoptotic protein depending on the extent of its cleavage by caspases (2). At low levels of caspase activity, RasGAP is cleaved at position 455, generating an N-terminal fragment (fragment N) and a C-terminal fragment (fragment C). Fragment C alone can induce apoptosis, but this response is completely inhibited by fragment N (3). Fragment N appears to be a general blocker of apoptosis downstream of caspase activation because it inhibits caspase 9-induced cell death. At higher caspase activity, fragment N is further processed and Cleavage of fragment N abrogates its protective functions, and hence the second cleavage of RasGAP promotes apoptosis (4).
1. Yang, J.-Y., Michod, D., Walicki, J., and Widmann, C. (2004) Biochem. Pharmacol. 68, 1027
2. Yang, J.-Y., and Widmann, C. (2001) Mol. Cell. Biol. 21, 5346-5358
3. Yang, J.-Y., Michod, D., Walicki, J., Murphy, B. M., Kasibhatla, S., Martin, S., and Widmann, C. (2004) Mol. Cell. Biol. 24, 10425
4. Yang, J. Y., Walicki, J., Michod, D., Dubuis, G., and Widmann, C. (2005) Mol. Biol. Cell, 16, 3511
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