Linked Life Data

20724817

Source:http://linkedlifedata.com/resource/pubmed/id/20724817

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2010-9-20
pubmed:abstractText
A half century ago, the antagonistic pleiotropy (AP) theory had solved a mystery of aging, by postulating genes beneficial early in life at the cost of aging. Recently it was argued however that there are very few clear-cut examples of antagonistically pleiotropic (AP) genes other than p53. In contrast, here I discuss that p53 is not a clear-cut example of AP genes but is rather an aging-suppressor (gerosuppressor). In contrast, clear-cut examples of AP genes are genes that encode the TOR (target of rapamycin) pathway. TOR itself is the ultimate example of AP gene because its deletion is lethal in embryogenesis. Early in life the TOR pathway drives developmental program, which persists later in life as an aimless quasi-program of aging and age-related diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3151-6
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Revisiting the antagonistic pleiotropy theory of aging: TOR-driven program and quasi-program.
pubmed:affiliation
Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA. blagosklonny@oncotarget.com
pubmed:publicationType
Journal Article, Review