Reference: Sanchez Y, et al. (1996)
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Abstract
Mutants of the Saccharomyces cerevisiae ataxia telangiectasia mutated (ATM) homolog MEC1/SAD3/ESR1 were identified that could live only if the RAD53/SAD1 checkpoint kinase was overproduced. MEC1 and a structurally related gene, TEL1, have overlapping functions in response to DNA damage and replication blocks that in mutants can be provided by overproduction of RAD53. Both MEC1 and TEL1 were found to control phosphorylation of Rad53p in response to DNA damage. These results indicate that RAD53 is a signal transducer in the DNA damage and replication checkpoint pathways and functions downstream of two members of the ATM lipid kinase family. Because several members of this pathway are conserved among eukaryotes, it is likely that a RAD53-related kinase will function downstream of the human ATM gene product and play an important role in the mammalian response to DNA damage.
- Reference Type
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Journal Article |
Research Support, Non-U.S. Gov't |
Research Support, U.S. Gov't, P.H.S.
- Authors
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Sanchez Y,
Desany BA,
Jones WJ,
Liu Q,
Wang B,
Elledge SJ
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- TEL1 | MEC1 | RAD53
Gene Ontology Annotations
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Regulator | Target | Direction | Regulation Of | Happens During | Method | Evidence |
TEL1 | RAD53 | | protein activity | DNA damage response | manually curated | qualitative western immunoblotting evidence |
MEC1 | RAD53 | | protein activity | DNA damage response | manually curated | qualitative western immunoblotting evidence |
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