Data sheet
| Size | 100ug/vial |
| Storage | At -20C for one year. After reconstitution, at 4C for one month. |
| Form | lyophilized |
| Ig type | rabbit IgG |
| Immunogen/Antigen | A synthetic peptide corresponding to a sequence at the N-terminal |
| Reconstitution | 0.2ml of distilled water will yield a concentration of 500μg/ml. |
More info
Background
PEBP1(Phosphatidylethanolamine-binding protein 1), also called PBP, RKIP, inhibits the phosphorylation and activation of MEK by RAF1. PEBP1 is identical to the phosphatidylethanolamine-binding protein (PBP) with a relative molecular mass of 23 kD. The PEBP1 gene is mapped on 12q24.23. PEBP1 coimmunoprecipitates with RAF1 and MEK from cell lysates and colocalizes with RAF1 when examined by confocal microscopy. PEBP1 overexpression interferes with the activation of MEK and ERK, induction of AP1-dependent reporter genes, and transformation elicited by an oncogenically activated RAF1 kinase. PEBP1 expression was rapidly upregulated during induction of chemotherapy-triggered apoptosis in human prostate and breast cancer cell lines, and maximal RKIP expression correlated perfectly with the onset of apoptosis by Chatterjee et al(2004). RKIP depletion decreased the mitotic index, the number of metaphase cells, traversal times from nuclear envelope breakdown to anaphase, and an override of mitotic checkpoints induced by spindle poisons.
PEBP1(Phosphatidylethanolamine-binding protein 1), also called PBP, RKIP, inhibits the phosphorylation and activation of MEK by RAF1. PEBP1 is identical to the phosphatidylethanolamine-binding protein (PBP) with a relative molecular mass of 23 kD. The PEBP1 gene is mapped on 12q24.23. PEBP1 coimmunoprecipitates with RAF1 and MEK from cell lysates and colocalizes with RAF1 when examined by confocal microscopy. PEBP1 overexpression interferes with the activation of MEK and ERK, induction of AP1-dependent reporter genes, and transformation elicited by an oncogenically activated RAF1 kinase. PEBP1 expression was rapidly upregulated during induction of chemotherapy-triggered apoptosis in human prostate and breast cancer cell lines, and maximal RKIP expression correlated perfectly with the onset of apoptosis by Chatterjee et al(2004). RKIP depletion decreased the mitotic index, the number of metaphase cells, traversal times from nuclear envelope breakdown to anaphase, and an override of mitotic checkpoints induced by spindle poisons.