PMID: 11901208Mar 20, 2002Paper

p75-nerve growth factor as an antiapoptotic complex: independence versus cooperativity in protection from enediyne chemotherapeutic agents

Molecular Pharmacology
Chaohua YanNina F Schor

Abstract

Growth factors, including nerve growth factor (NGF), have been hypothesized to play a role in resistance to chemotherapeutic agent-induced apoptosis. Induction by NGF of resistance to apoptosis is primarily thought to be the result of its binding to its high-affinity receptor, TrkA. The low-affinity NGF receptor, p75, has long been thought merely to facilitate NGF binding to TrkA. However, we have previously shown that the binding of NGF to its low-affinity receptor, p75, protects neuroblastoma cells that do not express TrkA against apoptosis induced by enediyne chemotherapeutic agents. In cells that express both receptors, it is not clear what determines which receptor is responsible for the protective effect of NGF. We now show that, in enediyne-treated SH-SY5Y neuroblastoma transfectants with native levels of p75 and a low TrkA/p75 ratio (1/100), the anti-apoptotic effect of NGF requires binding to p75. In contrast, in transfectants with native levels of p75 and a high TrkA/p75 ratio (100/100), NGF treatment prevents enediyne-induced apoptosis by a mechanism independent of p75 binding. Treatment of low TrkA/p75 ratio cells with NGF results in activation and nuclear translocation of NF-kappaB and tyrosine phosphorylation of T...Continue Reading

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Citations

Aug 25, 2009·Cancer Chemotherapy and Pharmacology·Muriel BassiliH Uri Saragovi
Jan 15, 2013·Cancer Chemotherapy and Pharmacology·Veena GaneshanNina F Schor
Jun 6, 2003·Cytokine & Growth Factor Reviews·Shahrooz Rabizadeh, Dale E Bredesen
Sep 10, 2011·Oxidative Medicine and Cellular Longevity·Alliya QaziNina F Schor
Dec 15, 2010·Pediatric Research·Christopher A IngrahamNina F Schor
Jun 23, 2011·Paediatric Drugs·Veena R Ganeshan, Nina F Schor
Nov 21, 2013·Cancer Chemotherapy and Pharmacology·Veena R Ganeshan, Nina F Schor
Dec 3, 2014·Oral Oncology·Joseph RohSufi M Thomas
Oct 13, 2009·Experimental Cell Research·Christopher A Ingraham, Nina F Schor
May 22, 2009·Journal of Neurochemistry·Zhiping MiNina Felice Schor
Nov 1, 2011·British Journal of Clinical Pharmacology·Salvatore SalomoneFilippo Drago
Jul 12, 2005·Neurobiology of Disease·Zeljka Korade MirnicsNina F Schor
Apr 5, 2016·Annals of Neurology·Nancy RatnerNina F Schor
Jun 22, 2005·Brain Research. Molecular Brain Research·Chaohua YanNina Felice Schor
Aug 29, 2003·Oncogene·Ljubica IvanisevicH Uri Saragovi
Sep 14, 2018·Archives of Dermatological Research·Min ZhangYongqian Cao
Nov 22, 2005·Progress in Neurobiology·Nina Felice Schor

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis