Hervouet 2006 Biochem Biophys Res Commun: Difference between revisions

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|authors=Hervouet E, Pecina P, Demont J, Vojtíšková A, Simonnet H, Houštek J, Godinot C
|authors=Hervouet E, Pecina P, Demont J, Vojtíšková A, Simonnet H, Houštek J, Godinot C
|year=2006
|year=2006
|journal=Biochem Biophys Res Commun.
|journal=Biochem. Biophys. Res. Commun.
|abstract=Cobalt is often used as a hypoxia mimic in cell culture, because it stabilizes the α subunits of the transcription factor, HIF (hypoxia-inducible factor). We have previously shown that HIF stabilization due to a deficiency of the von Hippel Lindau protein (pVHL) in clear cell renal carcinoma (CRCC) was correlated to a down-regulation of oxidative phosphorylation. To better understand this mechanism, we have used CoCl2 in CRCC expressing stably transfected ''vhl''. We show that, in addition to its effect on HIF-α subunits, CoCl2 prevented the normal processing of the precursor of cytochrome ''c''  oxidase (COX) subunit 4 and induced COX degradation very likely by inhibiting the mitochondrial intermediate peptidase (MIP) that cleaves the COX4 precursor protein. This cobalt-induced MIP inhibition was however not observed in other human mitochondrial precursor sequences as previously predicted from comparison between human and yeast mitochondrial precursor sequences.
|abstract=Cobalt is often used as a hypoxia mimic in cell culture, because it stabilizes the α subunits of the transcription factor, HIF (hypoxia-inducible factor). We have previously shown that HIF stabilization due to a deficiency of the von Hippel Lindau protein (pVHL) in clear cell renal carcinoma (CRCC) was correlated to a down-regulation of oxidative phosphorylation. To better understand this mechanism, we have used CoCl2 in CRCC expressing stably transfected ''vhl''. We show that, in addition to its effect on HIF-α subunits, CoCl2 prevented the normal processing of the precursor of cytochrome ''c''  oxidase (COX) subunit 4 and induced COX degradation very likely by inhibiting the mitochondrial intermediate peptidase (MIP) that cleaves the COX4 precursor protein. This cobalt-induced MIP inhibition was however not observed in other human mitochondrial precursor sequences as previously predicted from comparison between human and yeast mitochondrial precursor sequences.
|keywords=Hypoxia-inducible factor, Cytochrome ''c'' oxidase subunit 4, Cytochrome ''c'' oxidase biogenesis, Mitochondrial precursor processing, Mitochondrial intermediate peptidase, Cobalt chloride, ''Homo sapiens'', [[Saccharomyces cerevisiae]]
|keywords=Hypoxia-inducible factor, Cytochrome ''c'' oxidase subunit 4, Cytochrome ''c'' oxidase biogenesis, Mitochondrial precursor processing, Mitochondrial intermediate peptidase, Cobalt chloride, ''Homo sapiens'', [[Saccharomyces cerevisiae]]

Revision as of 13:51, 30 September 2010

Publications in the MiPMap
Hervouet E, Pecina P, Demont J, Vojtíšková A, Simonnet H, Houštek J, Godinot C (2006) Inhibition of cytochrome c oxidase subunit 4 precursor processing by the hypoxia mimic cobalt chloride. Biochem Biophys Res Commun. 344(4):1086-93.


Hervouet E, Pecina P, Demont J, Vojtíšková A, Simonnet H, Houštek J, Godinot C (2006) Biochem. Biophys. Res. Commun.

Abstract: Cobalt is often used as a hypoxia mimic in cell culture, because it stabilizes the α subunits of the transcription factor, HIF (hypoxia-inducible factor). We have previously shown that HIF stabilization due to a deficiency of the von Hippel Lindau protein (pVHL) in clear cell renal carcinoma (CRCC) was correlated to a down-regulation of oxidative phosphorylation. To better understand this mechanism, we have used CoCl2 in CRCC expressing stably transfected vhl. We show that, in addition to its effect on HIF-α subunits, CoCl2 prevented the normal processing of the precursor of cytochrome c oxidase (COX) subunit 4 and induced COX degradation very likely by inhibiting the mitochondrial intermediate peptidase (MIP) that cleaves the COX4 precursor protein. This cobalt-induced MIP inhibition was however not observed in other human mitochondrial precursor sequences as previously predicted from comparison between human and yeast mitochondrial precursor sequences. Keywords: Hypoxia-inducible factor, Cytochrome c oxidase subunit 4, Cytochrome c oxidase biogenesis, Mitochondrial precursor processing, Mitochondrial intermediate peptidase, Cobalt chloride, Homo sapiens, Saccharomyces cerevisiae


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Stress:Cancer; Apoptosis; Cytochrome c"Cancer; Apoptosis; Cytochrome c" 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., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" 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. 



Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


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