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J Med Dent Sci. 1998 Jun;45(2):141-9.

Analysis of downstream effectors of p53 on cell growth arrest and apoptosis induced by a temperature-sensitive Val138 mutant.

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Department of Molecular & Cellular Oncology and Microbiology, Faculty of Dentistry, Tokyo Medical & Dental University, Japan.


To elucidate the mechanism for cell growth arrest in relation to apoptosis mediated by the p53 gene, I studied two p53-null human cancer cell lines (K562 and Jurkat) carrying a human p53 temperature sensitive (ts) mutant (p53138val). The cell growth in the newly established K562 cells carrying the ts mutant was arrested in G0/G1 at the permissive temperature (32.5 degrees C) , at least in part, due to induction of p21/waf1. In apoptosis-induced Jurkat cells upon temperature shift-down, a lower level of p21 induction relative to that of MDM2 was observed in comparison with that in K562 cells. Meanwhile, levels of bax and bcl-2 expression were relatively constant upon temperature shift-down in both cell lines. Studies on the phosphorylation pattern of Rb family proteins, and results of gel-shift and antibody super-shift assays showed the accumulation of Rb/E2F complexes in growth-arrested K562 cells, but no such phenomenon was observed in Jurkat cells. Taken together, the results are consistent with the idea that a higher level of p21 expression and its subsequent Rb/E2F complex formation played an important role in the growth arrest of K562 cells.

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