2015
DOI: 10.1155/2016/8752821
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Induction of Expression of p75 Neurotrophin Receptor Intracellular Domain Does Not Induce Expression or Enhance Activity of Mitochondrial Complex II

Abstract: Fenretinide is a chemotherapeutic agent in clinical trials for the treatment of neuroblastoma, among the most common and most deadly cancers of childhood. Fenretinide induces apoptosis in neuroblastoma cells through accumulation of mitochondrial reactive oxygen species released from Complex II. The neurotrophin receptor, p75NTR, potentiates this effect. The signaling activity of p75NTR is dependent upon its cleavage to its intracellular domain, p75ICD, trafficking of p75ICD to the nucleus, and functioning of p… Show more

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Cited by 3 publications
(4 citation statements)
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“…p75NTR ICD exerts several functions, ranging from survival to cell death, in relation to the co-receptors and/or the type of ligands [ 68 ]. In addition, recent reports indicated that p75NTR ICD may translocate to the nucleus, possibly regulating gene expression [ 7 , 68 , 69 , 70 ].…”
Section: Neurotrophins: From Cell Signaling To Metabolic Processesmentioning
confidence: 99%
“…p75NTR ICD exerts several functions, ranging from survival to cell death, in relation to the co-receptors and/or the type of ligands [ 68 ]. In addition, recent reports indicated that p75NTR ICD may translocate to the nucleus, possibly regulating gene expression [ 7 , 68 , 69 , 70 ].…”
Section: Neurotrophins: From Cell Signaling To Metabolic Processesmentioning
confidence: 99%
“…Subsequently, we checked for putative molecular mechanisms explaining the proNGF-induced metabolic shift. Experimental evidence highlights that both p75NTR FL and p75ICD may translocate to the nucleus and regulate gene transcription [ 30 , 36 ]. Furthermore, NGF/proNGF stimulation enhances p75NTR processing and translocation into the nuclear compartment [ 37 ].…”
Section: Resultsmentioning
confidence: 99%
“…Also, induction of p75NTR expression does not result in a consistent change across neuroblastoma cell lines in expression of the retinoid binding protein, CRABP-I. 31,32 Potentiation by p75NTR of redox stress and apoptosis induction by 4-HPR requires p38MAPK phosphorylation, JNK phosphorylation, caspase 3 activation, Akt cleavage, and a decrease in Akt phosphorylation. 29 It is hypothesized that this pro-apoptotic signaling cascade enhances the generation or half-life of mitochondrial reactive oxygen species at the level of complex II.…”
Section: ■ Asymmetric Dimethylargininementioning
confidence: 91%
“…This enhancement does not involve induction of overexpression or increased activity of complex II. Also, induction of p75NTR expression does not result in a consistent change across neuroblastoma cell lines in expression of the retinoid binding protein, CRABP-I. , …”
Section: Redox Signaling As a Targetmentioning
confidence: 92%