Polyclonal Antibody to Raf-1
Figure 1: Western blot analysis of extract from mouse brain tissue and C6 cells using Raf-1 Antibody 35-1757
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Shipping Info:
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| Format : | Purified |
| Amount : | 100 µl |
| Isotype : | Rabbit IgG |
| Content : | Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. |
| Storage condition : | Store the antibody at 4°C, stable for 6 months. For long-term storage, store at -20°C. Avoid repeated freeze and thaw cycles. |
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). 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
Predicted MW: 74kd, Western blotting: 1:500~1:1000
For Research Use Only. Not for use in diagnostic/therapeutics procedures.
| Subcellular location: | Cytoplasm, Cell membrane, Mitochondrion, Nucleus |
| Post transnational modification: | Methylated in response to EGF treatment. This modification leads to destabilization of the protein, possibly through proteasomal degradation (By similarity). |
| BioGrid: | 246833. 7 interactions. |
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