Difference between revisions of "Tello 2011 Cell Metab"
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{{Labeling | {{Labeling | ||
|area=Respiration, Genetic knockout; overexpression | |||
|organism=Mouse | |organism=Mouse | ||
|model cell lines=Fibroblast | |model cell lines=Fibroblast | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|enzymes=Complex I | |enzymes=Complex I | ||
|injuries=Anaerobic metabolism, Hypoxia, RONS; Oxidative Stress | |injuries=Anaerobic metabolism, Hypoxia, RONS; Oxidative Stress | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Revision as of 12:13, 9 August 2013
| Tello D, Balsa E, Acosta-Iborra B, Fuertes-Yebra E, Elorza A, Ordóñez Á, Corral-Escariz M, Soro I, López-Bernardo E, Perales-Clemente E, Martínez-Ruiz A, Enríquez JA, Aragonés J, Cadenas S, Landázuri MO (2011) Induction of the mitochondrial NDUFA4L2 protein by HIF-1α decreases oxygen consumption by inhibiting Complex I activity. Cell Metab 14: 768-779. |
Tello D, Balsa E, Acosta-Iborra B, Fuertes-Yebra E, Elorza A, Ordonez A, Corral-Escariz M, Soro I, Lopez-Bernardo E, Perales-Clemente E, Martinez-Ruiz A, Enriquez JA, Aragones J, Cadenas S, Landazuri MO (2011) Cell Metab
Abstract: The fine regulation of mitochondrial function has proved to be an essential metabolic adaptation to fluctuations in oxygen availability. During hypoxia, cells activate an anaerobic switch that favors glycolysis and attenuates the mitochondrial activity. This switch involves the hypoxia-inducible transcription factor-1 (HIF-1). We have identified a HIF-1 target gene, the mitochondrial NDUFA4L2 (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex, 4-like 2). Our results, obtained employing NDUFA4L2-silenced cells and NDUFA4L2 knockout murine embryonic fibroblasts, indicate that hypoxia-induced NDUFA4L2 attenuates mitochondrial oxygen consumption involving inhibition of Complex I activity, which limits the intracellular ROS production under low-oxygen conditions. Thus, reducing mitochondrial Complex I activity via NDUFA4L2 appears to be an essential element in the mitochondrial reprogramming induced by HIF-1. • Keywords: hypoxia-inducible transcription factor-1 (HIF-1)
• O2k-Network Lab: ES Madrid Cadenas S
Labels: MiParea: Respiration, Genetic knockout; overexpression"Genetic knockout; overexpression" is not in the list (Respiration, Instruments;methods, mt-Biogenesis;mt-density, mt-Structure;fission;fusion, mt-Membrane, mtDNA;mt-genetics, nDNA;cell genetics, Genetic knockout;overexpression, Comparative MiP;environmental MiP, Gender, ...) of allowed values for the "MiP area" property.
Stress:Anaerobic metabolism"Anaerobic metabolism" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Hypoxia, RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Mouse
Preparation: Intact cells Enzyme: Complex I
HRR: Oxygraph-2k
