Document Detail


Evolutionarily conserved regulation of TOR signaling.
MedLine Citation:
PMID:  23698095     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The target of rapamycin (TOR) is an evolutionarily conserved protein kinase that regulates cell growth in response to various environmental as well as intracellular cues through the formation of two distinct TOR complexes (TORC), TORC1 and TORC2. Dysregulation of TORC1 and TORC2 activity is closely associated with various diseases, including diabetes, cancer, and neurodegenerative disorders. Over the past few years, new regulatory mechanisms of TORC1 and TORC2 activity have been elucidated. Furthermore, recent advances in the study of TOR inhibitors have revealed previously unrecognized cellular functions of TORC1. In this review, we briefly summarize the current understanding of the evolutionarily conserved TOR signaling from upstream regulators to downstream events.
Authors:
Terunao Takahara; Tatsuya Maeda
Related Documents :
23916475 - The activation of p2y6 receptor in cultured spinal microglia induces the production of ...
12684495 - Circadian and photic regulation of phosphorylation of erk1/2 and elk-1 in the suprachia...
23892075 - Oscillatory enzyme reactions and michaelis-menten kinetics.
23929665 - Rational design of resorcylic acid lactone analogues as covalent mnk1/2 kinase inhibito...
18405665 - The vacuolar v1/v0-atpase is involved in the release of the hops subunit vps41 from vac...
8692805 - Disruption of the macmarcks gene prevents cranial neural tube closure and results in an...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-5-21
Journal Detail:
Title:  Journal of biochemistry     Volume:  -     ISSN:  1756-2651     ISO Abbreviation:  J. Biochem.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-5-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376600     Medline TA:  J Biochem     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Institute of Molecular and Cellular Biosciences, The University of Tokyo.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  New insights into extracellular and post-translational regulation of TGF-? family signalling pathway...
Next Document:  Generation of membrane diversity by lysophospholipid acyltransferases.