The lack of G1/S arrest in teratocarcinoma F9 cells is due to degradation of p21WAF1/CIP1 protein

A. B. Malashicheva, T. V. Kislyakova, V. A. Pospelov

Результат исследований: Научные публикации в периодических изданияхстатья


We have studied the ability of F9 teratocarcinoma cells to arrest in G1/S and G2/M checkpoints following γ-irradiation. Wild-type p53 protein is rapidly accumulated in F9 cells after γ-irradiation, however this is not followed by G1/S arrest; there is just a reversible delay of the cell cycle in G2/M. In order to elucidate the reasons of the lack of G1/S arrest in F9 cells we investigated the levels of regulatory cell cycle proteins: G1-cyclins, cyclin dependent kinases and kinase inhibitor p21WAF1/CIP1. We have shown that in spite of p53-dependent activation of P21WAF1/CIP1 promoter, P21WAF1/CIP1 protein is not revealed by different polyclonal and monoclonal antibodies, either by immunoblotting or by immunofluorescent staining. However, when cells are treated with specific proteasome inhibitor lactacystin, p21WAF1/CIP1 protein is revealed. We therefore suggest that p21WAF1/CIP1 protein is subjected to proteasome degradation in F9 cells and probably the lack of G1/S arest after γ-irradiation is due to this degradation. Thus, it is the combination of functionally active p53 with low level expression of p21WAF1/CIP2 that causes a short delay of the cell cycle progression in G2/M, rather than the G1-arrest after γ-irradiation of F9 cells.

Язык оригиналаанглийский
Страницы (с-по)439-440
Число страниц2
Номер выпуска5
СостояниеОпубликовано - 1 дек 2000

Предметные области Scopus

  • Патология и судебная медицина
  • Гистология
  • Медицина (все)

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