YDR217C
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| Systematic name | YDR217C |
| Gene name | RAD9 |
| Aliases | |
| Feature type | ORF, Verified |
| Coordinates | Chr IV:903477..899548 |
| Primary SGDID | S000002625 |
Description of YDR217C: DNA damage-dependent checkpoint protein, required for cell-cycle arrest in G1/S, intra-S, and G2/M; transmits checkpoint signal by activating Rad53p and Chk1p; hyperphosphorylated by Mec1p and Tel1p; potential Cdc28p substrate[1][2]
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Contents
Community Commentary
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Alleles, Strains, and Phenotypes
Multiple Knockout Strains
Together with: DCC1, CTF8
Phenotype(s): Viable
ctf8 rad9 double deletion strain is defective in phosphorulation of Rad53p in responce to HU and MMS. [3] [4]
Together with: DCC1, CTF8
Phenotype(s): Viable
dcc1∆ rad9∆ double deletion strain is defective in phosphorylation of Rad53p and shows higher sensitivity to HU and MMS than WT and single mutant strains. [3] [4]
Protein Details
Protein Modification
Modification(s): Phosphorylation
Identified as an efficient substrate of Clb2-Cdk1-as1 in a screen of a proteomic GST-fusion library. [1] [5]
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References
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- ↑ 1.0 1.1 Ubersax JA, et al. (2003) Targets of the cyclin-dependent kinase Cdk1. Nature 425(6960):859-64 SGD PMID 14574415
- ↑ Toh GW and Lowndes NF (2003) Role of the Saccharomyces cerevisiae Rad9 protein in sensing and responding to DNA damage. Biochem Soc Trans 31(Pt 1):242-6 SGD PMID 12546694
- ↑ 3.0 3.1 Pan X, et al. (2006) A DNA integrity network in the yeast Saccharomyces cerevisiae. Cell 124(5):1069-81 SGD PMID 16487579
- ↑ 4.0 4.1 submitted by Shin-ichiro Hiraga on 2006-06-20
- ↑ submitted by Jeff Ubersax on 2004-01-21
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