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GENES & DEVELOPMENT 20:3337-3341, 2006
©2006 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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PERSPECTIVE

HIF and MIF—a nifty way to delay senescence?

Amit Maity and Constantinos Koumenis1

Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA

The first 100 words of the full text of this article appear below.

Normal mammalian cells have a finite replicative life span. This rather simple observation, which has profound implications for the biology of aging and cancer, was made several decades ago by Hayflick who found that isolated human fibroblasts grown in culture could not divide indefinitely (Hayflick and Moorhead 1961Go). After a number of cell divisions (now known as the "Hayflick limit"), cells slowed down their division cycle and acquired a more "flattened" morphology, eventually becoming nondividing, yet viable cells. This process was termed cellular senescence and its many facets, triggers, and consequences for multicellular organisms have only recently begun to . . . [Full Text of this Article]


   ‘Replicative’ and ‘premature’ cellular senescence
 

   HIF-1 and its regulation of the hypoxic response of MIF
 

   MIF
 

   HIF, senenscence, and radiation response
 

   Therapeutic implications
 

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Related Article

HIF1{alpha} delays premature senescence through the activation of MIF
Scott M. Welford, Barbara Bedogni, Katarina Gradin, Lorenz Poellinger, Marianne Broome Powell, and Amato J. Giaccia
Genes & Dev. 2006 20: 3366-3371. [Abstract] [Full Text] [PDF]





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