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© 2015 Elsevier B.V. Stable overexpression of endothelial nitric oxide synthase (NOS-3) in HepG2 cells (4TO-NOS) leads to increased nitro-oxidative stress and upregulation of the cell death mediators p53 and Fas. Thus, NOS-3 overexpression has been suggested as a useful antiproliferative mechanism in hepatocarcinoma cells. We aimed to identify the underlying mechanism of cell death induced by NOS-3 overexpression at basal conditions and with anti-Fas treatment. The intracellular localization of NOS-3, the nitro-oxidative stress and the mitochondrial activity were analysed. In addition, the protein expression profile in 4TO-NOS was screened for differentially expressed proteins potentially involved in the induction of apoptosis. NOS-3 localization in the mitochondrial outer membrane was not associated with changes in the respiratory cellular capacity, but was related to the mitochondrial biogenesis increase and with a higher protein expression of mitochondrial complex IV. Nitro-oxidative stress and cell death in NOS-3 overexpressing cells occurred with the expression increase of pro-apoptotic genes and a higher expression/activity of the enzymes adrenodoxin reductase mitochondrial (AR) and cathepsin D (CatD). CatD overexpression in 4TO-NOS was related to the apoptosis induction independently of its catalytic activity. In addition, CatD activity inhibition by pepstatin A was not effective in blocking apoptosis induced by anti-Fas. In summary, NOS-3 overexpression resulted in an increased sensitivity to anti-Fas induced cell death, independently of AR expression and CatD activity.

Pertenece a

Digital.CSIC  

Autor(es)

Linares, clara I -  Sánchez -  Aragó, María -  Cuezva, José M. -  Mata, Manuel de la - 

Id.: 70715047

Idioma: eng  - 

Versión: 1.0

Estado: Final

Palabras claveFas -  mediated apoptosis - 

Tipo de recurso: Artículo  - 

Tipo de Interactividad: Expositivo

Nivel de Interactividad: muy bajo

Audiencia: Estudiante  -  Profesor  -  Autor  - 

Estructura: Atomic

Coste: no

Copyright: sí

: openAccess

Requerimientos técnicos:  Browser: Any - 

Relación: [References] Publisher's version
[References] Sí

Fecha de contribución: 17-ene-2018

Contacto:

Localización:
* doi: 10.1016/j.bbamcr.2015.02.015
* issn: 1879-2596
* Biochimica et Biophysica Acta - Molecular Cell Research 1853: 1182- 1194 (2015)
* 10.1016/j.bbamcr.2015.02.015

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