PMID- 18240421
OWN - NLM
STAT- MEDLINE
DCOM- 20080215
LR  - 20211008
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1773
IP  - 12
DP  - 2007 Dec
TI  - Regulation of mitochondrial oxidative phosphorylation through cell signaling.
PG  - 1701-20
AB  - The mitochondrial oxidative phosphorylation (OxPhos) system plays a key role in 
      energy production, the generation of free radicals, and apoptosis. A lack of 
      cellular energy, excessive radical production, and dysregulated apoptosis are 
      found alone or in combination in most human diseases, including neurodegenerative 
      diseases, stroke, cardiovascular disorders, ischemia/reperfusion, and cancer. In 
      the context of its relevance to human disease, this article reviews current 
      knowledge about the regulation of OxPhos with a focus on cell signaling and 
      discusses identified phosphorylation sites with the aid of crystal structures of 
      OxPhos complexes. Several recent studies have shown that all OxPhos components 
      can be phosphorylated; even the small electron carrier cytochrome c is tyrosine 
      phosphorylated in vivo. We propose that in higher organisms, in contrast to 
      bacteria, cell signaling pathways are the main regulator of energy production, 
      triggered for example by hormones. Pathways that have been identified to act on 
      OxPhos include protein kinases A and C and growth factor activated receptor 
      tyrosine kinase signaling. Present knowledge about kinases and phosphatases that 
      execute signals at the level of the mitochondrial OxPhos system, and newly 
      emerging concepts, such as the translocation of kinases to the mitochondria upon 
      stimulation of a signaling pathway, are discussed.
FAU - Huttemann, Maik
AU  - Huttemann M
AD  - Center for Molecular Medicine and Genetics, Wayne State University School of 
      Medicine, Detroit, MI 48201, USA. mhuttema@med.wayne.edu
FAU - Lee, Icksoo
AU  - Lee I
FAU - Samavati, Lobelia
AU  - Samavati L
FAU - Yu, Hong
AU  - Yu H
FAU - Doan, Jeffrey W
AU  - Doan JW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Humans
MH  - Mitochondria/enzymology/*metabolism
MH  - Neoplasms/metabolism/pathology
MH  - Neurodegenerative Diseases/metabolism/pathology
MH  - *Oxidative Phosphorylation
MH  - *Signal Transduction
RF  - 202
EDAT- 2008/02/02 09:00
MHDA- 2008/02/19 09:00
CRDT- 2008/02/02 09:00
PHST- 2008/02/02 09:00 [pubmed]
PHST- 2008/02/19 09:00 [medline]
PHST- 2008/02/02 09:00 [entrez]
AID - S0167-4889(07)00236-4 [pii]
AID - 10.1016/j.bbamcr.2007.10.001 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2007 Dec;1773(12):1701-20. doi: 
      10.1016/j.bbamcr.2007.10.001.