Source: | Rabbit | Gene Id: | 369 |
Isotype: | IgG | Swiss Prot: | P10398 |
purity: | Affinity purification |
Background: |
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). |
Reactivity | Human |
Tested applications | WB IHC |
Clonality | Polyclonal Antibody |
Calculated MW | 68 kDa |
Recommended Dilutions |
WB 1:500-1:1000
IHC 1:50-1:100
|
Immunogen | A synthetic peptide of human ARAF |
Storage | Store at -20°C or -80°C in PBS with 0.02% sodium azide and 50% glycerol. Avoid freeze/thaw cycles. |
Synonym | PKS2, A-RAF, ARAF1, RAFA1 |
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