Tipping the balance toward longevity.
Genetic experiments in C. elegans suggested that SIR2, an NAD-dependent protein deacetylase, acts through FOXO/DAF-16 transcription factor to prolong life. Recent studies show that mammalian SIR2 deacetylates FOXO, and may maximize survival by tempering cell death and increasing stress resistance.
Antebi
Adam
A
Max-Planck-Institut für molekulare Genetik, Ihnestrasse 73, D-14195 Berlin, Germany.
D000818:Animals; D017173:Caenorhabditis elegans; D029742:Caenorhabditis elegans Proteins; D016923:Cell Death / Q000235:genetics / Q000502:physiology*; D051858:Forkhead Transcription Factors; D020868:Gene Silencing; D008136:Longevity / Q000235:genetics / Q000502:physiology*; D037761:Sirtuins / Q000378:metabolism / Q000502:physiology*; D014157:Transcription Factors / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D029742:Caenorhabditis elegans Proteins; D051858:Forkhead Transcription Factors; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; C108831:daf-16 protein, C elegans; D037761:Sirtuins