Función biológica de IF1, el inhibidor de la ATP sintasa mitocondrial

SCIENTIFIC AREA
Molecular Oncology
CENTER
Centro de Biología Molecular “Severo Ochoa” CSIC-UAM (CBMSO)
VACANCIES
1
CONTACT E-MAIL
jmcuezva@cbm.csic.es
DESCRIPTION OF THE OFFER

Temática en relación con los siguientes trabajos:

Santacatterina F, et al., Down-regulation of oxidative phosphorylation in the liver by expression of the ATPase inhibitory factor 1 induces a tumor-promoter metabolic state. Oncotarget. 2016 Jan 5;7(1):490-508. 

García-Bermúdez J, et al.,PKA Phosphorylates the ATPase Inhibitory Factor 1 and Inactivates Its Capacity to Bind and Inhibit the Mitochondrial H(+)-ATP Synthase. Cell Rep. 2015 Sep 29;12(12):2143-55.

Formentini L, et al., In vivo inhibition of the mitochondrial H+-ATP synthase in neurons promotes metabolic preconditioning. EMBO J. 2014 Apr 1;33(7):762-78.
 
Sánchez-Aragó M, et al., Degradation of IF1 controls energy metabolism during osteogenic differentiation of stem cells. EMBO Rep. 2013 Jul;14(7):638-44.
 
Sánchez-Aragó M, et al., Expression, regulation and clinical relevance of the ATPase inhibitory factor 1 in human cancers. Oncogenesis. 2013 Apr 22;2:e46.

Formentini L, et al., The mitochondrial ATPase inhibitory factor 1 triggers a ROS-mediated retrograde prosurvival and proliferative response. Mol Cell. 2012 Mar 30;45(6):731-42.

MASTER
Biomolecules & Cell D.
Molecular Biomedicine