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Difference between revisions of "Havlickova 2010 Biochim Biophys Acta"

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(Created page with "{{Publication |title=Havlíčková V, Kaplanová V, Nůsková H, Drahota Z, Houštěk J (2009) Knockdown of F1 epsilon subunit decreases mitochondrial content of ATP synthase 2 a...")
 
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|year=2009
|year=2009
|journal=Biochim. Biophys. Acta
|journal=Biochim. Biophys. Acta
|abstract=The subunit ε of mitochondrial ATP synthase is the only F1 subunit without a homolog in bacteria and chloroplasts and represents the least characterized F1 subunit of the mammalian enzyme. Silencing of the ATP5E gene in HEK293 cells resulted in downregulation of the activity and content of the mitochondrial ATP synthase complex and of ADP-stimulated respiration to approximately 40% of the control. The decreased content of the ε subunit was paralleled by a decrease in the F1 subunits α and β and in the Fo subunits a and d while the content of the subunit c was not affected. The subunit c was present in the full-size ATP synthase complex and in subcomplexes of 200–400 kDa that neither contained the F1 subunits, nor the Fo subunits. The results indicate that the ε subunit is essential for the assembly of F1 and plays an important role in the incorporation of the hydrophobic subunit c into the F1-c oligomer rotor of the mitochondrial ATP synthase complex.
|abstract=The subunit ε of mitochondrial ATP synthase is the only F1 subunit without a homolog in bacteria and chloroplasts and represents the least characterized F1 subunit of the mammalian enzyme. Silencing of the ''ATP5E'' gene in HEK293 cells resulted in downregulation of the activity and content of the mitochondrial ATP synthase complex and of ADP-stimulated respiration to approximately 40% of the control. The decreased content of the ε subunit was paralleled by a decrease in the F1 subunits α and β and in the Fo subunits a and d while the content of the subunit c was not affected. The subunit c was present in the full-size ATP synthase complex and in subcomplexes of 200–400 kDa that neither contained the F1 subunits, nor the Fo subunits. The results indicate that the ε subunit is essential for the assembly of F1 and plays an important role in the incorporation of the hydrophobic subunit c into the F1-c oligomer rotor of the mitochondrial ATP synthase complex.
|keywords=Mitochondria,  ATP synthase, Epsilon subunit, c subunit, Biogenesis
|keywords=Mitochondria,  ATP synthase, Epsilon subunit, C subunit, Biogenesis
}}
}}
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Revision as of 13:53, 2 November 2010

Publications in the MiPMap
Havlíčková V, Kaplanová V, Nůsková H, Drahota Z, Houštěk J (2009) Knockdown of F1 epsilon subunit decreases mitochondrial content of ATP synthase 2 and leads to accumulation of subunit c. Biochimica et Biophysica Acta. 1797: 1124-1129.


Havličkova V, Kaplanova V, Nůskova H, Drahota Z, Houštek J (2009) Biochim. Biophys. Acta

Abstract: The subunit ε of mitochondrial ATP synthase is the only F1 subunit without a homolog in bacteria and chloroplasts and represents the least characterized F1 subunit of the mammalian enzyme. Silencing of the ATP5E gene in HEK293 cells resulted in downregulation of the activity and content of the mitochondrial ATP synthase complex and of ADP-stimulated respiration to approximately 40% of the control. The decreased content of the ε subunit was paralleled by a decrease in the F1 subunits α and β and in the Fo subunits a and d while the content of the subunit c was not affected. The subunit c was present in the full-size ATP synthase complex and in subcomplexes of 200–400 kDa that neither contained the F1 subunits, nor the Fo subunits. The results indicate that the ε subunit is essential for the assembly of F1 and plays an important role in the incorporation of the hydrophobic subunit c into the F1-c oligomer rotor of the mitochondrial ATP synthase complex. Keywords: Mitochondria, ATP synthase, Epsilon subunit, C subunit, Biogenesis


Labels:

Stress: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. 


Enzyme: Complex V; ATP Synthase"Complex V; ATP Synthase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" 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. 


HRR: Oxygraph-2k