Regulating mammalian checkpoints through Cdc25 inactivation. - Test2 - elhamkhani - TriplyDB

Regulating mammalian checkpoints through Cdc25 inactivation.

Regulating mammalian checkpoints through Cdc25 inactivation.

http://www.wikidata.org/entity/Q28387035

about

MicroRNAs in the DNA Damage/Repair Network and Cancer Impaired DNA damage checkpoint response in MIF-deficient mice Cdc2: a monopotent or pluripotent CDK?Chk1 phosphorylation of Metnase enhances DNA repair but inhibits replication fork restart DNA damage activates a spatially distinct late cytoplasmic cell-cycle checkpoint network controlled by MK2-mediated RNA stabilization Differential roles for checkpoint kinases in DNA damage-dependent degradation of the Cdc25A protein phosphatase Maintaining Genome Stability in Defiance of Mitotic DNA Damage Coordination of DNA damage tolerance mechanisms with cell cycle progression in fission yeast.SCFbeta-TRCP links Chk1 signaling to degradation of the Cdc25A protein phosphatase Checkpoint kinase 1 in DNA damage response and cell cycle regulation Status of p53 in human cancer cells does not predict efficacy of CHK1 kinase inhibitors combined with chemotherapeutic agents Cell-cycle checkpoints and cancer Phospho-Ser/Thr-binding domains: navigating the cell cycle and DNA damage response Fission yeast Clp1p phosphatase affects G2/M transition and mitotic exit through Cdc25p inactivation Antitumor activity of di-n-butyl-(2,6-difluorobenzohydroxamato)tin(IV) against human gastric carcinoma SGC-7901 cells via G2/M cell cycle arrest and cell apoptosis Transcriptional regulation is a major controller of cell cycle transition dynamics An essential role for the RNA-binding protein Smaug during the Drosophila maternal-to-zygotic transition.cdc-25.4, a Caenorhabditis elegans Ortholog of cdc25, Is Required for Male Mating Behavior Chk1, but not Chk2, inhibits Cdc25 phosphatases by a novel common mechanism.Cdk2 is required for p53-independent G2/M checkpoint control.RSK promotes G2/M transition through activating phosphorylation of Cdc25A and Cdc25B Alpha-santalol, a chemopreventive agent against skin cancer, causes G2/M cell cycle arrest in both p53-mutated human epidermoid carcinoma A431 cells and p53 wild-type human melanoma UACC-62 cells.NPRL2 sensitizes human non-small cell lung cancer (NSCLC) cells to cisplatin treatment by regulating key components in the DNA repair pathway.Caffeine and human DNA metabolism: the magic and the mystery.Transforming growth factor beta facilitates beta-TrCP-mediated degradation of Cdc25A in a Smad3-dependent manner.Beta-TrCP recognizes a previously undescribed nonphosphorylated destruction motif in Cdc25A and Cdc25B phosphatases.A general framework for modeling growth and division of mammalian cells Human Cdc14B promotes progression through mitosis by dephosphorylating Cdc25 and regulating Cdk1/cyclin B activity.Interaction of a 14-3-3 protein with the plant microtubule-associated protein EDE1 Loss of cytoplasmic CDK1 predicts poor survival in human lung cancer and confers chemotherapeutic resistance Cell cycle G2/M arrest through an S phase-dependent mechanism by HIV-1 viral protein R.Regulation of HuR by DNA Damage Response Kinases.Novel 9'-substituted-noscapines: synthesis with Suzuki cross-coupling, structure elucidation and biological evaluation Prophase I arrest and progression to metaphase I in mouse oocytes: comparison of resumption of meiosis and recovery from G2-arrest in somatic cells Phosphatases in the cellular response to DNA damage.Design, synthesis and biological evaluation of 3,5-disubstituted 2-amino thiophene derivatives as a novel class of antitumor agents.Activation of cell cycle arrest and apoptosis by the proto-oncogene Pim-2.CDK2 and PKA mediated-sequential phosphorylation is critical for p19INK4d function in the DNA damage response Mek1 kinase governs outcomes of meiotic recombination and the checkpoint response.Development of synthetic lethality anticancer therapeutics.

P2860

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P2860

Regulating mammalian checkpoints through Cdc25 inactivation.

http://www.wikidata.org/entity/Q28387035

description

2003 nî lūn-bûn

@nan

2003 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2003 թվականի հուլիսին հրատարակված գիտական հոդված

@hy

2003年の論文

@ja

2003年論文

@yue

2003年論文

@zh-hant

2003年論文

@zh-hk

2003年論文

@zh-mo

2003年論文

@zh-tw

2003年论文

@wuu

name

Regulating mammalian checkpoints through Cdc25 inactivation

@nl

Regulating mammalian checkpoints through Cdc25 inactivation.

@ast

Regulating mammalian checkpoints through Cdc25 inactivation.

@en

type

label

Regulating mammalian checkpoints through Cdc25 inactivation

@nl

Regulating mammalian checkpoints through Cdc25 inactivation.

@ast

Regulating mammalian checkpoints through Cdc25 inactivation.

@en

prefLabel

Regulating mammalian checkpoints through Cdc25 inactivation

@nl

Regulating mammalian checkpoints through Cdc25 inactivation.

@ast

Regulating mammalian checkpoints through Cdc25 inactivation.

@en

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Regulating mammalian checkpoints through Cdc25 inactivation.

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Giulio F Draetta

http://www.w3.org/2001/XMLSchema#string

Maddalena Donzelli

http://www.w3.org/2001/XMLSchema#string

P2860

Linkage of ATM to cell cycle regulation by the Chk2 protein kinase

Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome

Arsenite-induced Cdc25C Degradation is through the KEN-box and Ubiquitin-proteasome Pathway

The ATM-Chk2-Cdc25A checkpoint pathway guards against radioresistant DNA synthesis

Human wee1 maintains mitotic timing by protecting the nucleus from cytoplasmically activated Cdc2 kinase

Specific activation of cdc25 tyrosine phosphatases by B-type cyclins: evidence for multiple roles of mitotic cyclins

Interaction of 14-3-3 with signaling proteins is mediated by the recognition of phosphoserine

Plk1 promotes nuclear translocation of human Cdc25C during prophase

Disruption of the checkpoint kinase 1/cell division cycle 25A pathway abrogates ionizing radiation-induced S and G2 checkpoints.

CDC25A phosphatase is a target of E2F and is required for efficient E2F-induced S phase

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671-677

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scholarly article

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10.1038/SJ.EMBOR.EMBOR887

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