Hervouet 2006 Biochem Biophys Res Commun: Difference between revisions

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{{Publication
{{Publication
|title=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.  
|title=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 344:1086-93.
|authors=Hervouet E, Pecina P, Demont J, Vojtíšková A, Simonnet H, Houštek J, Godinot C
|authors=Hervouet E, Pecina P, Demont J, Vojtiskova A, Simonnet H, Houstek 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''
|mipnetlab=CZ Prague Houstek J
|discipline=Biomedicine
}}
}}
{{Labeling
{{Labeling
|area=Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression
|diseases=Cancer
|organism=Human, Saccharomyces cerevisiae, Fungi
|preparations=Intact cells
|enzymes=Complex IV;cytochrome c oxidase
|topics=Inhibitor
|couplingstates=ROUTINE
|instruments=Oxygraph-2k
|discipline=Biomedicine
|discipline=Biomedicine
|injuries=Cancer; Apoptosis; Cytochrome c, Genetic Defect; Knockdown; Overexpression
|kinetics=Inhibitor; Uncoupler
|topics=Respiration; OXPHOS; ETS Capacity
|instruments=Oxygraph-2k, Chemicals; Media, Method
|articletype=Protocol; Manual
}}
}}

Latest revision as of 14:30, 26 March 2018

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 344:1086-93.


Hervouet E, Pecina P, Demont J, Vojtiskova A, Simonnet H, Houstek 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

O2k-Network Lab: CZ Prague Houstek J


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression  Pathology: Cancer 

Organism: Human, Saccharomyces cerevisiae, Fungi 

Preparation: Intact cells  Enzyme: Complex IV;cytochrome c oxidase  Regulation: Inhibitor  Coupling state: ROUTINE 

HRR: Oxygraph-2k 


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