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      Early aging and age-related pathologies in mice deficient in BMAL1, the core componentof the circadian clock.

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          Abstract

          Mice deficient in the circadian transcription factor BMAL1 (brain and muscle ARNT-like protein) have impaired circadian behavior and demonstrate loss of rhythmicity in the expression of target genes. Here we report that Bmal1(-/-) mice have reduced lifespans and display various symptoms of premature aging including sarcopenia, cataracts, less subcutaneous fat, organ shrinkage, and others. The early aging phenotype correlates with increased levels of reactive oxygen species in some tissues of the Bmal1(-/- )animals. These findings, together with data on CLOCK/BMAL1-dependent control of stress responses, may provide a mechanistic explanation for the early onset of age-related pathologies in the absence of BMAL1.

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          Author and article information

          Journal
          Genes Dev
          Genes & development
          Cold Spring Harbor Laboratory
          0890-9369
          0890-9369
          Jul 15 2006
          : 20
          : 14
          Affiliations
          [1 ] Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, Ohio 44195, USA. kondrar@ccf.org
          Article
          20/14/1868
          10.1101/gad.1432206
          1522083
          16847346
          64b20f02-5135-4d5d-b000-70b22c451a93
          History

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