PMID- 21487027
OWN - NLM
STAT- MEDLINE
DCOM- 20110810
LR  - 20211203
IS  - 1548-9221 (Electronic)
IS  - 1548-9213 (Print)
IS  - 1548-9221 (Linking)
VI  - 26
IP  - 2
DP  - 2011 Apr
TI  - mTor signaling in skeletal muscle during sepsis and inflammation: where does it 
      all go wrong?
PG  - 83-96
LID - 10.1152/physiol.00044.2010 [doi]
AB  - The mammalian target of rapamycin (mTOR) is an evolutionarily conserved protein 
      kinase that exquisitely regulates protein metabolism in skeletal muscle. mTOR 
      integrates input from amino acids, growth factors, and intracellular cues to make 
      or break muscle protein. mTOR accomplishes this task by stimulating the 
      phosphorylation of substrates that control protein translation while 
      simultaneously inhibiting proteasomal and autophagic protein degradation. In a 
      metabolic twist of fate, sepsis induces muscle atrophy in part by the aberrant 
      regulation of mTOR. In this review, we track the steps of normal mTOR signaling 
      in muscle and examine where they go astray in sepsis and inflammation.
FAU - Frost, Robert A
AU  - Frost RA
AD  - Department of Cellular and Molecular Physiology, Pennsylvania State University 
      College of Medicine, Hershey, Pennsylvania, USA.
FAU - Lang, Charles H
AU  - Lang CH
LA  - eng
GR  - R01 GM038032/GM/NIGMS NIH HHS/United States
GR  - GM-38032/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United States
TA  - Physiology (Bethesda)
JT  - Physiology (Bethesda, Md.)
JID - 101208185
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Inflammation/metabolism/pathology
MH  - Muscle, Skeletal/*metabolism/pathology
MH  - Myositis/*metabolism/pathology
MH  - Sepsis/*metabolism/pathology
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC3606812
MID - NIHMS449771
EDAT- 2011/04/14 06:00
MHDA- 2011/08/11 06:00
PMCR- 2013/03/24
CRDT- 2011/04/14 06:00
PHST- 2011/04/14 06:00 [entrez]
PHST- 2011/04/14 06:00 [pubmed]
PHST- 2011/08/11 06:00 [medline]
PHST- 2013/03/24 00:00 [pmc-release]
AID - 26/2/83 [pii]
AID - 10.1152/physiol.00044.2010 [doi]
PST - ppublish
SO  - Physiology (Bethesda). 2011 Apr;26(2):83-96. doi: 10.1152/physiol.00044.2010.