- CITATIONS: 1
|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||21057 Da|
|Other Names||Phosphatidylethanolamine-binding protein 1, PEBP-1, HCNPpp, Neuropolypeptide h3, Prostatic-binding protein, Raf kinase inhibitor protein, RKIP, Hippocampal cholinergic neurostimulating peptide, HCNP, PEBP1, PBP, PEBP|
|Target/Specificity||A synthetic peptide corresponding to residues in human RKIP was used as an 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||RKIP Antibody Phospho (pS153) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Binds ATP, opioids and phosphatidylethanolamine. Has lower affinity for phosphatidylinositol and phosphatidylcholine. Serine protease inhibitor which inhibits thrombin, neuropsin and chymotrypsin but not trypsin, tissue type plasminogen activator and elastase (By similarity). Inhibits the kinase activity of RAF1 by inhibiting its activation and by dissociating the RAF1/MEK complex and acting as a competitive inhibitor of MEK phosphorylation.|
Provided below are standard protocols that you may find useful for product applications.
Raf kinase inhibitory protein (RKIP) belongs to the phosphatidylethanolamine-binding protein (PEBP) family. It is an inhibitor of the Raf/MEK/MAP kinase signaling cascade and is a suppressor of cancer metastasis (1). RKIP is involved in neural development, cardiac function and spermatogenesis and appears to have serine protease activity. The inhibition Raf-1-mediated phosphorylation of MEK results from RKIP binding to Raf-1. Dysregulated RKIP expression has the potential to contribute to pathophysiological processes including Alzheimer's disease and diabetic nephropathy (2). RKIP represents a novel effector of signal transduction pathways leading to apoptosis and a prognostic marker of the pathogenesis of human cancer cells and tumors (3).
1. Eves EM, et al. Mol Cell. 23(4):561-74, 2006
2. Keller E T, et al. Biochemical pharmacology 68(6):1049-1053, 2004
3. Chatterjee D, et al. J Biol Chem. 279(17):17515-23, 2004
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