Research Program for Receptor Biochemistry and Tumor Metabolism

Salzburg, Austria

Research Program for Receptor Biochemistry and Tumor Metabolism

Salzburg, Austria
SEARCH FILTERS
Time filter
Source Type

Mueller E.E.,Research Program for Receptor Biochemistry and Tumor Metabolism | Mayr J.A.,Research Program for Receptor Biochemistry and Tumor Metabolism | Zimmermann F.A.,Research Program for Receptor Biochemistry and Tumor Metabolism | Feichtinger R.G.,Research Program for Receptor Biochemistry and Tumor Metabolism | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2012

Mitochondrial DNA (mtDNA) depletion syndromes are generally associated with reduced activities of oxidative phosphorylation (OXPHOS) enzymes that contain subunits encoded by mtDNA. Conversely, entirely nuclear encoded mitochondrial enzymes in these syndromes, such as the tricarboxylic acid cycle enzyme citrate synthase (CS) and OXPHOS complex II, usually exhibit normal or compensatory enhanced activities. Here we report that a human cell line devoid of mtDNA (HEK293 ρ 0 cells) has diminished activities of both complex II and CS. This finding indicates the existence of a feedback mechanism in ρ 0 cells that downregulates the expression of entirely nuclear encoded components of mitochondrial energy metabolism. © 2011 Elsevier Inc.


PubMed | Research Program for Receptor Biochemistry and Tumor Metabolism
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2012

Mitochondrial DNA (mtDNA) depletion syndromes are generally associated with reduced activities of oxidative phosphorylation (OXPHOS) enzymes that contain subunits encoded by mtDNA. Conversely, entirely nuclear encoded mitochondrial enzymes in these syndromes, such as the tricarboxylic acid cycle enzyme citrate synthase (CS) and OXPHOS complex II, usually exhibit normal or compensatory enhanced activities. Here we report that a human cell line devoid of mtDNA (HEK293 (0) cells) has diminished activities of both complex II and CS. This finding indicates the existence of a feedback mechanism in (0) cells that downregulates the expression of entirely nuclear encoded components of mitochondrial energy metabolism.

Loading Research Program for Receptor Biochemistry and Tumor Metabolism collaborators
Loading Research Program for Receptor Biochemistry and Tumor Metabolism collaborators