Linked Life Data

12424797

Source:http://linkedlifedata.com/resource/pubmed/id/12424797

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-11-8
pubmed:abstractText
In C. elegans, insulin-like hormone signal pathway plays a significant role in longevity. In particular, daf-16 gene product is indispensable factor for this lifespan-extension. This signal pathway is critical for dauer formation, which is a similar state to hibernation in mammals. We examined the expression level of mammalian daf-16 homologues, Foxo 1,3, and 4 (FKHR, FKHRL1, and AFX) mRNAs in the rat skeletal muscles during aging and in 30% caloric restricted of ad libitum fed. The expression level of AFX mRNA was significantly higher at 6 and 12 months than at 3 and 26 months, and FKHRL1 expression was significantly higher at 6 months than at 3 and 26 months but FKHR expression showed no significant change with age. We observed a characteristic expression of AFX and FKHR mRNAs to be significantly higher in the second day in caloric restriction by every-other-day feeding than in ad libitum fed. This suggests that caloric restriction may increase the expression of FKHR-family genes and prevent the aging process in the skeletal muscles.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1059-910X
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
331-4
pubmed:dateRevised
2008-5-6
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Effects of aging and caloric restriction on the gene expression of Foxo1, 3, and 4 (FKHR, FKHRL1, and AFX) in the rat skeletal muscles.
pubmed:affiliation
Department of Molecular Genetics, National Institute for Longevity Sciences (NILS), Aichi, Japan. tfuruyam@nils.go.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't