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A more recent version of this article appeared on July 1, 2002
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Submitted on October 31, 2001
Revised on March 6, 2002
Accepted on April 5, 2002
1 Department of Pharmacology, University of Pittsburgh School of Medicine, Biomedical Science Tower (BST) E1356, Pittsburgh, PA 15261
2 Department of Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461; and The Division of Hormone-Dependent Tumor Biology, The Albert Einstein Cancer Center, Bronx, NY 10461
* Corresponding author. E-mail address: feg5{at}pitt.edu.
Caveolae are vesicular invaginations of the plasma membrane. Caveolin-1 is the principal structural component of caveolae in vivo. Several lines of evidence are consistent with the idea that caveolin-1 functions as "transformation suppressor" protein. In fact, caveolin-1 mRNA and protein expression are lost or reduced during cell transformation by activated oncogenes. Interestingly, the human caveolin-1 gene is localized to a suspected tumor suppressor locus (7q31.1). We have previously demonstrated that over-expression of caveolin-1 arrests mouse embryonic fibroblasts in the G0/G1 phase of the cell cycle through activation of a p53/p21-dependent pathway, indicating a role of caveolin-1 in mediating growth arrest. However, it remains unknown whether over-expression of caveolin-1 promotes cellular senescence in vivo.
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