14-3-3 mediated regulation of the tumor suppressor protein, RASSF1A.
作者： Haya Abu Ghazaleh , Renfred S. Chow , Sheryl L. Choo , Diana Pham , Jamie D. Olesen
DOI: 10.1007/S10495-009-0451-6
关键词:
摘要: Death receptor-dependent apoptosis is an important mechanism of growth control. It has been demonstrated that Ras association domain family protein 1A (RASSF1A) a tumor suppressor involved in death apoptosis. However, it unclear how RASSF1A-mediated cell initiated. We have now detailed 14-3-3 dependent regulation death. demonstrate basal RASSF1A with was lost following stimulation necrosis factor alpha (TNFα) or TNFα related inducing ligand (TRAIL). Subsequent to the loss association, associated modulator (MOAP-1) followed by receptor either 1 (TNF-R1) TRAIL (TRAIL-R1). required phosphorylation serine/threonine kinase, glycogen synthase kinase 3β (GSK-3β), on serine 175, 178, and 179. Mutation these critical serines resulted earlier recruitment MOAP-1, TNF-R1, TRAIL-R1. Furthermore, stable cells containing triple mutant [serine (S) 175 alanine (A) [S175A], S178A, S179A] increased death, enhanced Annexin V staining cleavage poly (ADP-ribose) polymerase (PARP) when compared wild type RASSF1A. is, therefore, tightly controlled association.
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