Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2. - Wikidata - wikimedia - TriplyDB

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

http://www.wikidata.org/entity/Q37235809

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MicroRNAs in the DNA Damage/Repair Network and Cancer Phosphorylation: the molecular switch of double-strand break repair DNA damage activates a spatially distinct late cytoplasmic cell-cycle checkpoint network controlled by MK2-mediated RNA stabilization P90 RSK arranges Chk1 in the nucleus for monitoring of genomic integrity during cell proliferation CHK1 inhibitors in combination chemotherapy: thinking beyond the cell cycle BRCT domains: easy as one, two, three DNA Repair and Cytokines: TGF-β, IL-6, and Thrombopoietin as Different Biomarkers of Radioresistance Rho GTPases: Novel Players in the Regulation of the DNA Damage Response?Targeting ATM-deficient CLL through interference with DNA repair pathways The DNA damage response induced by infection with human cytomegalovirus and other viruses What goes on must come off: phosphatases gate-crash the DNA damage response Structure-based design, discovery and development of checkpoint kinase inhibitors as potential anticancer therapies Phosphopeptide interactions with BRCA1 BRCT domains: More than just a motif The convergence of DNA damage checkpoint pathways and androgen receptor signaling in prostate cancer MicroRNA and signal transduction pathways in tumor radiation response p38- and MK2-dependent signalling promotes stress-induced centriolar satellite remodelling via 14-3-3-dependent sequestration of CEP131/AZI1 Therapeutic targeting of a robust non-oncogene addiction to PRKDC in ATM-defective tumors.Ubiquitylation, neddylation and the DNA damage response Chk2 regulates cell cycle progression during mouse oocyte maturation and early embryo development The acetyltransferase Tip60 is a critical regulator of the differentiation-dependent amplification of human papillomaviruses.Activation of p38 MAP kinase and JNK pathways by UVA irradiation ATM/ATR checkpoint activation downregulates CDC25C to prevent mitotic entry with uncapped telomeres A mitotic phosphorylation feedback network connects Cdk1, Plk1, 53BP1, and Chk2 to inactivate the G(2)/M DNA damage checkpoint Two 4N cell-cycle arrests contribute to cisplatin-resistance Toxic effect of silica nanoparticles on endothelial cells through DNA damage response via Chk1-dependent G2/M checkpoint Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition.VIP blockade leads to microcephaly in mice via disruption of Mcph1-Chk1 signaling The oxidative stress responsive transcription factor Pap1 confers DNA damage resistance on checkpoint-deficient fission yeast cells p38 MAPK/MK2-mediated induction of miR-34c following DNA damage prevents Myc-dependent DNA replication Adapting glycolysis to cancer cell proliferation: the MAPK pathway focuses on PFKFB3: Figure 1 The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.JNK-mediated phosphorylation of Cdc25C regulates cell cycle entry and G(2)/M DNA damage checkpoint.Induction of mitotic cell death by overriding G2/M checkpoint in endometrial cancer cells with non-functional p53.Down-regulation of tricarboxylic acid (TCA) cycle genes blocks progression through the first mitotic division in Caenorhabditis elegans embryos.Distinct phosphatases antagonize the p53 response in different phases of the cell cycle Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage RSK promotes G2/M transition through activating phosphorylation of Cdc25A and Cdc25B Mammalian TIMELESS is required for ATM-dependent CHK2 activation and G2/M checkpoint control.A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration.Ataxia telangiectasia mutated- and Rad3-related kinase drives both the early and the late DNA-damage response to the monofunctional antitumour alkylator S23906.

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Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

http://www.wikidata.org/entity/Q37235809

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

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scientific article published on 21 February 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

@en

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

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type

label

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

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Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

@nl

prefLabel

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

@en

Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

@nl

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J.CEB.2009.01.018

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Current Opinion in Cell Biology

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Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.

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H Christian Reinhardt

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Michael B Yaffe

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P2860

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

Cytoplasmic localization of tristetraprolin involves 14-3-3-dependent and -independent mechanisms

PRAK is essential for ras-induced senescence and tumor suppression

Crystal structure of the p38 alpha-MAPKAP kinase 2 heterodimer

MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks

RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins

RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly

Sequential modification of NEMO/IKKgamma by SUMO-1 and ubiquitin mediates NF-kappaB activation by genotoxic stress

TAO kinases mediate activation of p38 in response to DNA damage

ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage

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245-255

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scholarly article

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10.1016/J.CEB.2009.01.018

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21

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2009-02-21T00:00:00Z

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