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Inactivation of p53 and life span extension of human diploid fibroblasts by mot‐2
Author(s) -
Kaul Sunil C.,
Reddel Roger R.,
Sugihara Takashi,
Mitsui Youji,
Wadhwa Renu
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01594-5
Subject(s) - transfection , senescence , biology , phenotype , fibroblast , ploidy , suppressor , population , life span , microbiology and biotechnology , wi 38 , cell culture , cell , plasmid , vector (molecular biology) , genetics , gene , recombinant dna , medicine , environmental health , evolutionary biology
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 β‐galactosidase (SA‐β‐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‐β‐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.