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RAD17 homolog

Rad17, Rad24, hRad17
The protein encoded by this gene is highly similar to the gene product of Schizosaccharomyces pombe rad17, a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This protein shares strong similarity with DNA replication factor C (RFC), and can form a complex with RFCs. This protein binds to chromatin prior to DNA damage and is phosphorylated by the checkpoint kinase ATR following damage. This protein recruits the RAD1-RAD9-HUS1 checkpoint protein complex onto chromatin after DNA damage, which may be required for its phosphorylation. The phosphorylation of this protein is required for the DNA-damage-induced cell cycle G2 arrest, and is thought to be a critical early event during checkpoint signaling in DNA-damaged cells. Eight alternatively spliced transcript variants of this gene, which encode four distinct proteins, have been reported. Two pseudogenes, located on chromosomes 7 and 13, have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rad9, Chk2, Mec1, CAN, rad1
Papers on Rad17
Chemogenetic profiling identifies RAD17 as synthetically lethal with checkpoint kinase inhibition.
Ideker et al., San Diego, United States. In Oncotarget, Dec 2015
We identified eight interactions, including the Replication Factor C (RFC)-related protein RAD17.
Radioprotective effects of genistein on HL-7702 cells via the inhibition of apoptosis and DNA damage.
Yan et al., Shanghai, China. In Cancer Lett, Oct 2015
In contrast, high concentration of GEN (20 µM) demonstrated radiosensitizing characteristics through the promotion of apoptosis and chromosome aberration, impairment of DNA repair, up-regulation of GRP78, and down-regulation of HUS1, SIRT1, RAD17, RAD51 and RNF8.
Dysregulation of apoptotic pathway candidate genes and proteins in infertile azoospermia patients.
Singh et al., Benares, India. In Fertil Steril, Sep 2015
Expression of phosphorylated P53 at the S15 position and phosphorylated RAD17 at S635 was observed in cases with spermatogenic impairment at the translational level.
Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis.
Lee et al., San Antonio, United States. In Plos Genet, Feb 2015
Distinct from other cellular defects associated with deletion of HST3 and HST4 including thermo-sensitivity and elevated spontaneous mutagenesis, the BIR defect in hst3Δ hst4Δ cannot be offset by the deletion of RAD17 or MMS22, but rather by the loss of RTT109 or ASF1, or in combination with the H3K56R mutation, which also restores tolerance to replication stress in mrc1 mutants.
Regulation of ATRIP protein abundance by RAD9 in the DNA damage repair pathway.
Ding et al., Nanchang, China. In Cell Mol Biol (noisy-le-grand), 2014
A number of proteins act in concert with ATR to phosphorylate Chk1, including RAD17, the RAD9-RAD1-HUS1 complex, ATR/ATRIP and TopBp1.
Replication factor C is a more effective proliferating cell nuclear antigen (PCNA) opener than the checkpoint clamp loader, Rad24-RFC.
Bloom et al., Gainesville, United States. In J Biol Chem, 2012
fewer open clamp loader-clamp complexes are formed when PCNA is bound by Rad24-RFC than when bound by RFC.
The Saccharomyces cerevisiae RAD9, RAD17 and RAD24 genes are required for suppression of mutagenic post-replicative repair during chronic DNA damage.
Paulovich et al., Seattle, United States. In Dna Repair (amst), 2010
a novel role for members of the S-phase DNA damage checkpoint, RAD9, RAD17 and RAD24 in suppressing mutagenic post-replicative repair was described.
Ubiquitylation of the 9-1-1 checkpoint clamp is independent of rad6-rad18 and DNA damage.
Ulrich et al., London, United Kingdom. In Cell, 2010
Rad17, a subunit of the PCNA-like 9-1-1 checkpoint clamp is ubiquitylated; however, in contrast to previous results, modification of Rad17 is found to be independent of DNA damage, the Rad6-Rad18 complex.
Proteolysis of Rad17 by Cdh1/APC regulates checkpoint termination and recovery from genotoxic stress.
Wan et al., Pittsburgh, United States. In Embo J, 2010
Proteolysis of Rad17 by Cdh1/APC regulates checkpoint termination and recovery from genotoxic stress
Identification of sam4 as a rad24 allele in Schizosaccharomyces pombe.
Kawamukai et al., Matsue, Japan. In Biosci Biotechnol Biochem, 2009
Identification of sam4 as an allele of rad24.
Evaluating HapMap SNP data transferability in a large-scale genotyping project involving 175 cancer-associated genes.
Benítez et al., Madrid, Spain. In Hum Genet, 2006
We found that of the 21 genes that contained at least one block larger than 60 kb, nine (ATM, ATR, BRCA1, ERCC6, FANCC, RAD17, RAD50, RAD54B and XRCC4) belonged to the GO category "DNA repair".
Yeast 14-3-3 proteins.
Steensma et al., Leiden, Netherlands. In Yeast, 2006
The yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe both have two genes encoding 14-3-3 proteins, BMH1 and BMH2 and rad24 and rad25, respectively.
G2 checkpoint abrogators as anticancer drugs.
Kawabe, Numazu, Japan. In Mol Cancer Ther, 2004
Damaged DNA in humans is detected by sensor proteins (such as hHUS1, hRAD1, hRAD9, hRAD17, and hRAD26) that transmit a signal via ATR to CHK1, or by another sensor complex (that may include gammaH2AX, 53BP1, BRCA1, NBS1, hMRE11, and hRAD50), the signal of which is relayed by ATM to CHK2.
Recruitment of Mec1 and Ddc1 checkpoint proteins to double-strand breaks through distinct mechanisms.
Sugimoto et al., Nagoya, Japan. In Science, 2001
Continuous HO expression results in the phosphorylation of Rad53, which is dependent on products of the ataxia telangiectasia mutated-related MEC1 gene and other checkpoint genes, including DDC1, RAD9, and RAD24.
ATR/ATM-mediated phosphorylation of human Rad17 is required for genotoxic stress responses.
Wang et al., Durham, United States. In Nature, 2001
Here we demonstrate a direct regulatory linkage between the human Rad17 homologue (hRad17) and the checkpoint kinases, ATM and ATR.
Suppression of spontaneous chromosomal rearrangements by S phase checkpoint functions in Saccharomyces cerevisiae.
Kolodner et al., San Diego, United States. In Cell, 2001
Mutations in Saccharomyces cerevisiae RFC5, DPB11, MEC1, DDC2 MEC3, RAD53, CHK1, PDS1, and DUN1 increased the rate of genome rearrangements up to 200-fold whereas mutations in RAD9, RAD17, RAD24, BUB3, and MAD3 had little effect.
Saccharomyces Ku70, mre11/rad50 and RPA proteins regulate adaptation to G2/M arrest after DNA damage.
Haber et al., Waltham, United States. In Cell, 1998
Saccharomyces cells suffering a single unrepairable double-strand break (DSB) exhibit a long, but transient arrest at G2/M. hdf1 cells, lacking Ku70p, fail to escape from this RAD9/RAD17-dependent checkpoint.
Radiation checkpoints in model systems.
Carr, Burgess Hill, United Kingdom. In Int J Radiat Biol, 1994
In addition, the rad24 and rad25 genes of S. pombe (which are involved in the radiation checkpoint) encode functionally overlapping essential proteins that are highly conserved in mammalian cells.
Radiation-induced mitotic delay: a genetic characterization in the fission yeast.
Rowley, Salt Lake City, United States. In Radiat Res, 1992
Through an examination of such mutants it has been shown that the X-ray transition point and the p34cdc2 execution point are coincident; wee1- strains are not delayed by irradiation; and the radiation-sensitive mutants rad1-1, rad3-136, rad9-192, and rad17-W are not delayed by radiation or by inhibitors of DNA synthesis, including hydroxyurea.
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