Product Description
Raf 1 Antibody | 79-697 | ProSci
Host: Rabbit
Reactivity: Rat
Homology: N/A
Immunogen: Raf-1 antibody was raised against a peptide sequence around aa. 641-645 (T-S-P-R-L ) derived from Rat Raf-1.
Research Area: Other
Tested Application: WB
Application: Western Blot: 1:500~1:1000
Specificiy: This antibody detects endogenous level of total Raf-1 protein.
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 74 kDa
Validation: N/A
Isoform: N/A
Purification: Antibodies were purified by affinity-chromatography using epitope-specific peptide
Clonality: Polyclonal
Clone: N/A
Isotype: N/A
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Antibody supplied in phosphate buffered saline (without Mg2+ and Ca2+) , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Concentration: 1 mg/mL
Storage Condition: Store antibody at -20˚C for up to one year.
Alternate Name: Raf, c-RAF, RAF proto-oncogene serine/threonine-protein kinase
User Note: N/A
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) . 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