p66Shc: At the crossroad of oxidative stress and the genetics of aging

Sally Purdom, Qin Chen

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

The biology of aging has been mysterious for centuries. Removal of the p66Shc gene, which encodes an adaptor protein for cell signaling, extends lifespan by ∼30% in mice and confers resistance to oxidative stress. The absence of p66Shc correlates with reduced levels of apoptosis. Oxidants induce phosphorylation of serine36 on p66Shc, contributing to inactivation of members of the Forkhead transcription factor family, some of which appear to regulate the expression of antioxidant genes. The expression of p66Shc is regulated by the methylation status of its promoter. This leads us to hypothesize that increased methylation of the p66Shc promoter might contribute to the absence of its expression and therefore extended longevity in particular individuals.

Original languageEnglish (US)
Pages (from-to)206-210
Number of pages5
JournalTrends in Molecular Medicine
Volume9
Issue number5
DOIs
StatePublished - May 1 2003

Fingerprint

Methylation
Oxidative Stress
Forkhead Transcription Factors
Oxidants
Antioxidants
Phosphorylation
Apoptosis
Gene Expression
Genes
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

p66Shc : At the crossroad of oxidative stress and the genetics of aging. / Purdom, Sally; Chen, Qin.

In: Trends in Molecular Medicine, Vol. 9, No. 5, 01.05.2003, p. 206-210.

Research output: Contribution to journalArticle

@article{fc92772a2d0045a5819f6e19bb0d24bd,
title = "p66Shc: At the crossroad of oxidative stress and the genetics of aging",
abstract = "The biology of aging has been mysterious for centuries. Removal of the p66Shc gene, which encodes an adaptor protein for cell signaling, extends lifespan by ∼30{\%} in mice and confers resistance to oxidative stress. The absence of p66Shc correlates with reduced levels of apoptosis. Oxidants induce phosphorylation of serine36 on p66Shc, contributing to inactivation of members of the Forkhead transcription factor family, some of which appear to regulate the expression of antioxidant genes. The expression of p66Shc is regulated by the methylation status of its promoter. This leads us to hypothesize that increased methylation of the p66Shc promoter might contribute to the absence of its expression and therefore extended longevity in particular individuals.",
author = "Sally Purdom and Qin Chen",
year = "2003",
month = "5",
day = "1",
doi = "10.1016/S1471-4914(03)00048-0",
language = "English (US)",
volume = "9",
pages = "206--210",
journal = "Trends in Molecular Medicine",
issn = "1471-4914",
publisher = "Elsevier Limited",
number = "5",

}

TY - JOUR

T1 - p66Shc

T2 - At the crossroad of oxidative stress and the genetics of aging

AU - Purdom, Sally

AU - Chen, Qin

PY - 2003/5/1

Y1 - 2003/5/1

N2 - The biology of aging has been mysterious for centuries. Removal of the p66Shc gene, which encodes an adaptor protein for cell signaling, extends lifespan by ∼30% in mice and confers resistance to oxidative stress. The absence of p66Shc correlates with reduced levels of apoptosis. Oxidants induce phosphorylation of serine36 on p66Shc, contributing to inactivation of members of the Forkhead transcription factor family, some of which appear to regulate the expression of antioxidant genes. The expression of p66Shc is regulated by the methylation status of its promoter. This leads us to hypothesize that increased methylation of the p66Shc promoter might contribute to the absence of its expression and therefore extended longevity in particular individuals.

AB - The biology of aging has been mysterious for centuries. Removal of the p66Shc gene, which encodes an adaptor protein for cell signaling, extends lifespan by ∼30% in mice and confers resistance to oxidative stress. The absence of p66Shc correlates with reduced levels of apoptosis. Oxidants induce phosphorylation of serine36 on p66Shc, contributing to inactivation of members of the Forkhead transcription factor family, some of which appear to regulate the expression of antioxidant genes. The expression of p66Shc is regulated by the methylation status of its promoter. This leads us to hypothesize that increased methylation of the p66Shc promoter might contribute to the absence of its expression and therefore extended longevity in particular individuals.

UR - http://www.scopus.com/inward/record.url?scp=0038509964&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0038509964&partnerID=8YFLogxK

U2 - 10.1016/S1471-4914(03)00048-0

DO - 10.1016/S1471-4914(03)00048-0

M3 - Article

C2 - 12763525

AN - SCOPUS:0038509964

VL - 9

SP - 206

EP - 210

JO - Trends in Molecular Medicine

JF - Trends in Molecular Medicine

SN - 1471-4914

IS - 5

ER -