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26. To prevent cells with damaged DNA from passing through the G, checkpoint, AT

ID: 209960 • Letter: 2

Question

26. To prevent cells with damaged DNA from passing through the G, checkpoint, ATR or ATM Chk1 or Chk2, which then phosphorylate and a) phosphorylate; inhibit protein phosphatase Cdc25. phosphorylate; stimulate dephosphorylate; inhibit c. d. dephosphorylate; stimulate 27. Your answer to 26 has a specific affect on cdc25 (t modification and the fate of cdc25 affect co hat's obvious from the question). How does th mmitment to s (DNA replication)? Be specific! Do not just repeat what's written in #26!! (This is not about cdc45: it's about cdc25 function) ATM ATR are Kinases that Phosphory late hkychkz ous they Coh Cycle atrrest(atest) ATM: recomgunes dsDNA breake .ntio)

Explanation / Answer

When DNA damage occurs, then delay occurs in the cell cycle in G1, that occurs through several mechanisms.

1. It involves phosphorylation events that initiate with either kinase ATM (Ataxia telangiectasia mutated) or ATR (Ataxia Telangiectasia and Rad3 related), which act as sensors, depending on the type of damage. These kinases phosphorylate and activate the effector kinases Chk2 and Chk1, respectively, which in turn phosphorylate the phosphatase Cdc25A. As Cdc25A activates the cyclin E-CDK2 complex by removing inhibitory phosphates from CDK2, in the absence of Cdc25A, cyclin E-CDK2 remains inactive, and the cell remains in G1.

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