Induction of Expression of p75 Neurotrophin Receptor Intracellular Domain Does Not Induce Expression or Enhance Activity of Mitochondrial Complex II.
Oxid Med Cell Longev
; 2016: 8752821, 2016.
Article
en En
| MEDLINE
| ID: mdl-26640617
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 p75ICD as a transcription factor. Mitochondrial Complex II comprises 4 subunits, all of which are encoded by nuclear DNA. We therefore hypothesized that the fenretinide-potentiating effects of p75NTR are the result of transcriptional enrichment of Complex II by p75ICD. However, the present studies demonstrate that neither induced expression of p75ICD or its active fragments nor overexpression of p75NTR results in altered expression or activity of Complex II.
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Regulación de la Expresión Génica
/
Receptores de Factor de Crecimiento Nervioso
/
Proteínas Mitocondriales
/
Complejo II de Transporte de Electrones
/
Mitocondrias
Límite:
Animals
Idioma:
En
Revista:
Oxid Med Cell Longev
Asunto de la revista:
METABOLISMO
Año:
2016
Tipo del documento:
Article
País de afiliación:
Estados Unidos