Product Pathways - MAPK Signaling
Phospho-c-Raf (Ser338) (56A6) Rabbit mAb #9427
|9427S||100 µl (10 western blots)||---||In Stock||---|
|9427P||40 µl (4 western blots)||---||In Stock||---|
|9427||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||74||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Specificity / Sensitivity
Phospho-c-Raf (Ser338) (56A6) Rabbit mAb detects endogenous levels of c-Raf only when phosphorylated at Ser338.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding serine 338 of human Raf.
A-Raf, B-Raf, and c-Raf (Raf-1) are the main effectors recruited by GTP-bound Ras to activate the MEK-MAP kinase pathway (1). Activation of c-Raf is the best understood and involves phosphorylation at multiple activating sites including Ser338, Tyr341, Thr491, Ser494, Ser497, and Ser499 (2). p21-activated protein kinase (PAK) has been shown to phosphorylate c-Raf at Ser338 and the Src family phosphorylates Tyr341 to induce c-Raf activity (3,4). Ser338 of c-Raf corresponds to similar sites in A-Raf (Ser299) and B-Raf (Ser445), although this site is constitutively phosphorylated in B-Raf (5). Inhibitory 14-3-3 binding sites on c-Raf (Ser259 and Ser621) can be phosphorylated by Akt and AMPK, respectively (6,7). While A-Raf, B-Raf, and c-Raf are similar in sequence and function, differential regulation has been observed (8). Of particular interest, B-Raf contains three consensus Akt phosphorylation sites (Ser364, Ser428, and Thr439) and lacks a site equivalent to Tyr341 of c-Raf (8,9). Research studies have shown that the B-Raf mutation V600E results in elevated kinase activity and is commonly found in malignant melanoma (10). Six residues of c-Raf (Ser29, Ser43, Ser289, Ser296, Ser301, and Ser642) become hyperphosphorylated in a manner consistent with c-Raf inactivation. The hyperphosphorylation of these six sites is dependent on downstream MEK signaling and renders c-Raf unresponsive to subsequent activation events (11).
- Avruch, J. et al. (1994) Trends Biochem Sci 19, 279-83.
- Chong, H. et al. (2001) EMBO J 20, 3716-27.
- King, A.J. et al. (1998) Nature 396, 180-3.
- Fabian, J.R. et al. (1993) Mol Cell Biol 13, 7170-9.
- Mason, C.S. et al. (1999) EMBO J 18, 2137-48.
- Zimmermann, S. and Moelling, K. (1999) Science 286, 1741-4.
- Sprenkle, A.B. et al. (1997) FEBS Lett 403, 254-8.
- Marais, R. et al. (1997) J Biol Chem 272, 4378-83.
- Guan, K.L. et al. (2000) J Biol Chem 275, 27354-9.
- Davies, H. et al. (2002) Nature 417, 949-54.
- Dougherty, M.K. et al. (2005) Mol Cell 17, 215-24.
- Kajiya, M. et al. (2008) J Biol Chem 283, 16259-67. Applications: Western Blotting.
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For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
This antibody is developed, validated, and produced by CST using in part technology under license (granting certain rights including those under U.S. Patents No. 5,675,063 and 7,429,487) from Epitomics, Inc.