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FGF1 protects neuroblastoma SH-SY5Y cells from p53-dependent apoptosis through an intracrine pathway regulated by FGF1 phosphorylation.

Cell Death Dis. 2017; 
Pirou Caroline,Montazer-Torbati Fatemeh,Jah Nadège,Delmas Elisabeth,Lasbleiz Christelle,Mignotte Bernard,Renaud F
Products/Services Used Details Operation
Catalog Antibody The primary antibodies used in this study were: anti-FGF1 (AB-32-NA, R&D Systems), anti-His tag (A00186, GenScript, Piscataway, NJ, USA), anti-P-p53 (Ser-15) (9284S, Cell Signaling, Danvers, MA, USA), anti-PUMAα(N-19, Santa Cruz, Dallas, TX, USA), anti-Caspase-9 (5B4, Abcam, Cambridge, UK), anti-cleaved Caspase-3 (Asp175, Cell Signaling), anti-PARP (9542S, Cell Signaling) and anti-Actin (A2066, Sigma-Aldrich). Get A Quote

摘要

Neuroblastoma, a sympathetic nervous system tumor, accounts for 15% of cancer deaths in children. In contrast to most human tumors, p53 is rarely mutated in human primary neuroblastoma, suggesting impaired p53 activation in neuroblastoma. Various studies have shown correlations between fgf1 expression levels and both prognosis severity and tumor chemoresistance. As we previously showed that fibroblast growth factor 1 (FGF1) inhibited p53-dependent apoptosis in neuron-like PC12 cells, we initiated the study of the interaction between the FGF1 and p53 pathways in neuroblastoma. We focused on the activity of either extracellular FGF1 by adding recombinant rFGF1 in media, or of intracellular FGF1 by ove... More

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