Linked Life Data

21646374

Source:http://linkedlifedata.com/resource/pubmed/id/21646374

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2011-6-20
pubmed:abstractText
PGC-1? is a transcriptional coactivator that powerfully regulates many pathways linked to energy homeostasis. Specifically, PGC-1? controls mitochondrial biogenesis in most tissues but also initiates important tissue-specific functions, including fiber type switching in skeletal muscle and gluconeogenesis and fatty acid oxidation in the liver. We show here that S6 kinase, activated in the liver upon feeding, can phosphorylate PGC-1? directly on two sites within its arginine/serine-rich (RS) domain. This phosphorylation significantly attenuates the ability of PGC-1? to turn on genes of gluconeogenesis in cultured hepatocytes and in vivo, while leaving the functions of PGC-1? as an activator of mitochondrial and fatty acid oxidation genes completely intact. These phosphorylations interfere with the ability of PGC-1? to bind to HNF4?, a transcription factor required for gluconeogenesis, while leaving undisturbed the interactions of PGC-1? with ERR? and PPAR?, factors important for mitochondrial biogenesis and fatty acid oxidation. These data illustrate that S6 kinase can modify PGC-1? and thus allow molecular dissection of its functions, providing metabolic flexibility needed for dietary adaptation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1549-5477
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1232-44
pubmed:dateRevised
2011-8-31
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Separation of the gluconeogenic and mitochondrial functions of PGC-1{alpha} through S6 kinase.
pubmed:affiliation
Department of Cell Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural