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HUS1 checkpoint homolog

Hus1, hHus1
The protein encoded by this gene is a component of an evolutionarily conserved, genotoxin-activated checkpoint complex that is involved in the cell cycle arrest in response to DNA damage. This protein forms a heterotrimeric complex with checkpoint proteins RAD9 and RAD1. In response to DNA damage, the trimeric complex interacts with another protein complex consisting of checkpoint protein RAD17 and four small subunits of the replication factor C (RFC), which loads the combined complex onto the chromatin. The DNA damage induced chromatin binding has been shown to depend on the activation of the checkpoint kinase ATM, and is thought to be an early checkpoint signaling event. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2011] (from NCBI)
Top mentioned proteins: Rad9, rad1, CAN, p53, FAN
Papers on Hus1
An epigenetic signal encoded protection mechanism is activated by graphene oxide to inhibit its induced reproductive toxicity in Caenorhabditis elegans.
Wang et al., Nanjing, China. In Biomaterials, Feb 2016
For the underlying molecular mechanism of reproductive toxicity of GO, we raised a signaling cascade of HUS-1/CLK-2-CEP-1-EGL-1-CED-4-CED-3 to explain the roles of core apoptosis signaling pathway and DNA damage checkpoints.
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 the present study, we showed that low concentration of GEN (1.5 µM) protected L-02 cells against radiation damage via inhibition of apoptosis, alleviation of DNA damage and chromosome aberration, down-regulation of GRP78 and up-regulation of HERP, HUS1 and hHR23A.
Genome Protection by the 9-1-1 Complex Subunit HUS1 Requires Clamp Formation, DNA Contacts, and ATR Signaling-independent Effector Functions.
Weiss et al., Ithaca, United States. In J Biol Chem, Jul 2015
The RAD9A-HUS1-RAD1 (9-1-1) complex is a heterotrimeric clamp that promotes checkpoint signaling and repair at DNA damage sites.
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
As a member of the RAD9-HUS1-RAD1 (9-1-1) complex, it can sense DNA damage and recruit ATR to damage sites.
Reproductive Toxicity of Endosulfan: Implication From Germ Cell Apoptosis Modulated by Mitochondrial Dysfunction and Genotoxic Response Genes in Caenorhabditis elegans.
Xu et al., Hefei, China. In Toxicol Sci, May 2015
However, the apoptotic effects of endosulfan were blocked in mutants of cep-1(w40), egl-1(n487), and hus-1(op241), indicating conserved genotoxic response genes played an essential role in endosulfan-induced germ cell apoptosis.
HUS1 regulates in vivo responses to genotoxic chemotherapies.
Weiss et al., Ithaca, United States. In Oncogene, May 2015
Optimal ATR signaling requires the RAD9A-RAD1-HUS1 (9-1-1) complex, a toroidal clamp that is loaded at damage sites and scaffolds signaling and repair factors.
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.
Lifespan and Stress Resistance in Drosophila with Overexpressed DNA Repair Genes.
Moskalev et al., Moscow, Russia. In Sci Rep, 2014
Overexpressed genes included those involved in recognition of DNA damage (homologs of HUS1, CHK2), nucleotide and base excision repair (homologs of XPF, XPC and AP-endonuclease-1), and repair of double-stranded DNA breaks (homologs of BRCA2, XRCC3, KU80 and WRNexo).
[Role of DNA repair genes in radiation-induced changes of lifespan of Drosophila melanogaster].
Moskalev et al., In Radiats Biol Radioecol, 2014
Also, we investigated the resistance to acute gamma-radiation of Drosophila with conditional ubiquitous overexpression of genes that are involved in DNA damage recognition (homologues of GADD45, HUS1, CHK2), excision repair (homologues of XPF, XPC, AP-endonuclease-1) and double-strand break repair (homologues of BRCA2, XRCC3, KU80, WRNexo).
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.
9-1-1: PCNA's specialized cousin.
Jentsch et al., Oxford, United Kingdom. In Trends Biochem Sci, 2011
The HUS1 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
RAD9 regulates multiple cellular processes that influence genomic integrity, and for at least some of its functions the protein acts as part of a heterotrimeric complex bound to HUS1 and RAD1 proteins.
Casein kinase 2-dependent phosphorylation of human Rad9 mediates the interaction between human Rad9-Hus1-Rad1 complex and TopBP1.
Tsurimoto et al., Fukuoka, Japan. In Genes Cells, 2010
The HUS1 protein interacts with casein kinase 2.
Interaction between human mismatch repair recognition proteins and checkpoint sensor Rad9-Rad1-Hus1.
Lu et al., Baltimore, United States. In Dna Repair (amst), 2010
9-1-1 complex is a component of the mismatch repair involved in MNNG-induced damage response.
Rad17 plays a central role in establishment of the interaction between TopBP1 and the Rad9-Hus1-Rad1 complex at stalled replication forks.
Dunphy et al., Pasadena, United States. In Mol Biol Cell, 2010
Data show that Rad17 mediates the interaction of the Rad9-Hus1-Rad1 (9-1-1) complex with the ATR-activating protein TopBP1 in Xenopus egg extracts.
Molecular parameters of genome instability: roles of fragile genes at common fragile sites.
Huebner et al., Columbus, United States. In J Cell Biochem, 2008
Deficiency of genes involved in DNA damage checkpoint responses, such as ATR, CHK1, HUS1 leads to increased frequency of fragile site instability.
DNA repair.
Rose et al., Vancouver, Canada. In Wormbook, 2005
Both of these responses are regulated by checkpoint genes including mrt-2, hus-1, rad-5 and cep-1, the C. elegans ortholog of the human tumour suppressor p53.
Caenorhabditis elegans ABL-1 antagonizes p53-mediated germline apoptosis after ionizing irradiation.
Kolesnick et al., New York City, United States. In Nat Genet, 2004
Our findings delineate an apoptotic pathway antagonized by ABL-1, which requires sequentially the cell cycle checkpoint genes clk-2, hus-1 and mrt-2; the C. elegans p53 homolog, cep-1; and the genes encoding the components of the conserved apoptotic machinery, ced-3, ced-9 and egl-1.
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.
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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