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BID as a double agent in cell life and death
1Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel. atan.gross@weizmann.ac.il
Cell Cycle (Georgetown, Tex.)
|April 4, 2006
Summary
DNA damage activates ATM, which phosphorylates BID. This regulates BID
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- DNA damage triggers ATM and ATR kinases.
- These kinases initiate cell cycle arrest, DNA repair, or apoptosis.
- The BCL-2 family member BID is involved in apoptosis.
Purpose of the Study:
- To investigate the role of BID in DNA damage response.
- To explore the connection between ATM and BID.
- To understand BID's function in cell cycle regulation during genotoxic stress.
Main Methods:
- Western blotting to detect BID phosphorylation.
- Cell cycle analysis.
- Apoptosis assays.
Main Results:
- DNA damage induces ATM-mediated phosphorylation of BID.
- Phosphorylated BID promotes S phase arrest.
- BID plays a pro-survival role in response to DNA damage.
Conclusions:
- BID integrates signals from ATM, linking DNA damage response to cell fate decisions.
- BID has a novel pro-survival function in S phase arrest.
- BID coordinates genotoxic stress responses and apoptosis.
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