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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Nov 2015.

RAD9 Rad9p

Rad9, hRad9
This gene product is highly similar to Schizosaccharomyces pombe rad9, a cell cycle checkpoint protein required for cell cycle arrest and DNA damage repair. This protein possesses 3' to 5' exonuclease activity, which may contribute to its role in sensing and repairing DNA damage. It forms a checkpoint protein complex with RAD1 and HUS1. This complex is recruited by checkpoint protein RAD17 to the sites of DNA damage, which is thought to be important for triggering the checkpoint-signaling cascade. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Rad17, CAN, rad1, Hus1, Chk2
Papers using Rad9 antibodies
Bcl-xL Retrotranslocates Bax from the Mitochondria into the Cytosol
Takehara Tetsuo, In PLoS ONE, 2010
... The antibody against Rad9 was purchased from Abcam (Cambridge, UK) ...
Papers on Rad9
Incorporation of metabolic activation potentiates cyclophosphamide-induced DNA damage response in isogenic DT40 mutant cells.
Nakamura et al., Fujisawa, Japan. In Mutagenesis, Jul 2015
When DT40 cells and mutant cells were exposed to the preactivated CP, CP caused increased cytotoxicity in FANC-, RAD9-, REV3- and RAD18-mutant cells compared to isogenic wild-type cells.
Regulation of NEIL1 protein abundance by RAD9 is important for efficient base excision repair.
Lieberman et al., New York City, United States. In Nucleic Acids Res, Jun 2015
RAD9 participates in DNA damage-induced cell cycle checkpoints and DNA repair.
NONO regulates the intra-S-phase checkpoint in response to UV radiation.
Pentimalli et al., Napoli, Italy. In Oncogene, May 2015
Consistently, NONO is present at the sites of UV-induced DNA damage where it localizes to RAD9 foci.
DNA Damage Response Checkpoint Activation Drives KP1019 Dependent Pre-Anaphase Cell Cycle Delay in S. cerevisiae.
Miller et al., Memphis, United States. In Plos One, Dec 2014
Importantly, we also find that deletion of RAD9, a gene required for the DDR, blocks drug-dependent changes in cell cycle progression, thereby establishing a causal link between the DDR and phenotypes induced by KP1019.
A physical association between the human mutY homolog (hMYH) and DNA topoisomerase II-binding protein 1 (hTopBP1) regulates Chk1-induced cell cycle arrest in HEK293 cells.
Han et al., Seoul, South Korea. In Cell Biosci, Dec 2014
Moreover, we observed that hMYH was essential for the accumulation of hTopBP1 on damaged DNA, where hTopBP1 interacts with hRad9, a component of the Rad9-Hus1-Rad1 complex.
DNA damage response genes and the development of cancer metastasis.
Lieberman et al., New York City, United States. In Radiat Res, Feb 2014
Several genes that participate in the DNA damage response, such as RAD9, PARP1, BRCA1, ATM and TP53 have been associated with metastasis by a number of in vitro biochemical and cellular assays, by examining human tumor specimens by immunohistochemistry or by DNA genome-wide gene expression profiling.
Repair complexes of FEN1 endonuclease, DNA, and Rad9-Hus1-Rad1 are distinguished from their PCNA counterparts by functionally important stability.
Ivanov et al., Berkeley, United States. In Proc Natl Acad Sci U S A, 2012
Data show models for the ternary PCNA/FEN1/DNA and Rad9-Rad1-Hus1 (9-1-1 complex)/FEN1/DNA assemblies.
Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery.
Gasser et al., Basel, Switzerland. In Nat Cell Biol, 2012
show that recombination intermediates take longer to form in cells lacking Rad9
Contributions of Rad9 to tumorigenesis.
Lieberman et al., New York City, United States. In J Cell Biochem, 2012
A review of the many activities assigned to Rad9, and speculation as to which influence its function in tumor development.
9-1-1: PCNA's specialized cousin.
Jentsch et al., Oxford, United Kingdom. In Trends Biochem Sci, 2011
The RAD9 is loaded to damaged sites where it serves as a platform for the selective recruitment of checkpoint and repair proteins.
The role of RAD9 in tumorigenesis.
Zhu et al., New York City, United States. In J Mol Cell Biol, 2011
Interestingly, human RAD9 overproduction correlates with prostate cancer whereas deletion of Mrad9, the corresponding mouse gene, in keratinocytes leads to skin cancer.
Reduced mRNA and protein expression of the genomic caretaker RAD9A in primary fibroblasts of individuals with childhood and independent second cancer.
Galetzka et al., Mainz, Germany. In Plos One, 2010
Modulation of RAD9A and other cell cycle arrest and DNA repair proteins contribute to the risk of developing a second malignancy in childhood cancer patients.
Rad3-dependent phosphorylation of the checkpoint clamp regulates repair-pathway choice.
Wang et al., Stanford, United States. In Nat Cell Biol, 2007
Our findings reveal a new mechanism by which phosphorylation of Rad9 at Thr 225 regulates the choice of repair pathways for maintaining genomic integrity during the cell cycle.
The role of DNA damage response proteins at telomeres--an "integrative" model.
Slijepcevic, Kingston upon Hull, United Kingdom. In Dna Repair (amst), 2006
Recent studies indicate that three more proteins, namely BRCA1, hRad9 and PARP1 are involved in telomere maintenance.
ATM signaling and 53BP1.
Halazonetis et al., United States. In Radiother Oncol, 2005
One of the proteins that sense these chromatin structure changes is 53BP1, a DNA damage checkpoint protein conserved in all eukaryotes and the putative ortholog of the S. cerevisiae RAD9 protein.
SMC5 and SMC6 genes are required for the segregation of repetitive chromosome regions.
Aragón et al., London, United Kingdom. In Nat Cell Biol, 2005
We show that mutant smc5-6 and smc6-9 cells undergo an aberrant mitosis in which chromosome segregation of repetitive regions is impaired; this leads to DNA damage and RAD9-dependent activation of the Rad53 protein kinase.
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.
DNA helicase gene interaction network defined using synthetic lethality analyzed by microarray.
Boeke et al., Baltimore, United States. In Nat Genet, 2003
SGS1 and SRS2 have synthetic defects with MRC1 but not RAD9, suggesting that SGS1 and SRS2 function in a parallel pathway with MRC1 to transduce the DNA replication stress signal to the general DNA damage checkpoint pathway.
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
Studies in fission yeast implicate members of the Rad family of checkpoint proteins, which includes Rad17, Rad1, Rad9 and Hus1, as key early-response elements during the activation of both the DNA damage and replication checkpoints.
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