Authors: Kaula SC; Reddelb RR; Sugiharac T; Mitsuia Y; Wadhwac R
Abstract: Normal human lung fibroblasts were transfected with expression plasmids encoding mot-2, an hsp70 family member that is associated with the immortal phenotype. After the empty vector-transfected controls had become senescent and positive for senescence-associated beta-galactosidase (SA-beta-gal), the mot-2-expressing cells continued to proliferate for an additional 12-18 population doublings and showed a young cell morphology and much lower SA-beta-gal activity. The tumor suppressor p53 was found to be transcriptionally inactivated in life span-extended cells. We have thus shown for the first time that overexpression of mot-2 in normal human cells is able to permit their temporary escape from senescence.
Keywords: *Cell Aging; Cell Division; Cell Line; Cell Size; Diploidy; Fibroblasts/*cytology/enzymology/metabolism; HSP70 Heat-Shock Proteins/genetics/*metabolism; Half-Life; Humans; Lung; Mitochondrial Proteins; Transcription, Genetic/genetics; Transfection; Tumor Suppressor Protein p53/*antagonists & inhibitors/genetics/*metabolism; beta-Galactosidase/metabolism|
Journal: FEBS letters Volume: 474 Issue: 2-3 Pages: 159-64 Date: June 6, 2000 PMID: 10838077 |
Kaula SC, Reddelb RR, Sugiharac T, Mitsuia Y, Wadhwac R (2000) Inactivation of p53 and life span extension of human diploid fibroblasts by mot-2. FEBS letters 474: 159-64.
Comment on This Data Unit