作者: Veronique A. J. Smits , Maartje A. van Peer , Marieke A. G. Essers , Rob Klompmaker , Gert Rijksen
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摘要: Basic fibroblast growth factor (bFGF) has been shown to induce inhibition of the neuroepithelioma cell line SK-N-MC. Here we show that this occurs in G2. We bFGF is active on these cells during S and early G2 phase. Therefore, constitutes a rather unusual mechanism inhibition, because it generally believed become refractory extracellular signals after passage through restriction point. treatment inhibits Tyr-15 dephosphorylation cdc2 prevents activation Cdc25C, similar what seen upon G2DNA damage checkpoint. Interestingly, both DNA damage- bFGF-induced effects phosphorylation are reverted by caffeine. To confirm involvement pathways induced damage, generated tetracycline-regulatable SK-N-MC clones expressing Cdc25C-S216A. Expression Cdc25C mutant can revert rescue from block imposed bFGF. Taken together, data define factor-sensitive point most likely involves regulation phosphorylation.