DNA damage activates the SAC in an ATM/ATR-dependent manner, independently of the kinetochore. - Wikidata - wikimedia - TriplyDB

DNA damage activates the SAC in an ATM/ATR-dependent manner, independently of the kinetochore.

DNA damage activates the SAC in an ATM/ATR-dependent manner, independently of the kinetochore.

http://www.wikidata.org/entity/Q30443388

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CDK5RAP2 is required for spindle checkpoint function Shugoshin-2 is essential for the completion of meiosis but not for mitotic cell division in mice Simian virus 40 large T antigen disrupts genome integrity and activates a DNA damage response via Bub1 binding Bub3-BubR1-dependent sequestration of Cdc20Fizzy at DNA breaks facilitates the correct segregation of broken chromosomes TRAIP is involved in chromosome alignment and SAC regulation in mouse oocyte meiosis Phosphoproteomic Profiling Reveals Epstein-Barr Virus Protein Kinase Integration of DNA Damage Response and Mitotic Signaling Connecting the microtubule attachment status of each kinetochore to cell cycle arrest through the spindle assembly checkpoint.UV-C irradiation delays mitotic progression by recruiting Mps1 to kinetochores The DNA damage response pathway contributes to the stability of chromosome III derivatives lacking efficient replicators.Synthetic cytotoxicity: digenic interactions with TEL1/ATM mutations reveal sensitivity to low doses of camptothecin Chromosome rearrangements and aneuploidy in yeast strains lacking both Tel1p and Mec1p reflect deficiencies in two different mechanisms.DNA damage to a single chromosome end delays anaphase onset Compromised spindle assembly checkpoint due to altered expression of Ubch10 and Cdc20 in human papillomavirus type 16 E6- and E7-expressing keratinocytes Topoisomerase II- and condensin-dependent breakage of MEC1ATR-sensitive fragile sites occurs independently of spindle tension, anaphase, or cytokinesis.An S/T-Q cluster domain census unveils new putative targets under Tel1/Mec1 control.DNA damage response and spindle assembly checkpoint function throughout the cell cycle to ensure genomic integrity.Spindle Checkpoint Factors Bub1 and Bub2 Promote DNA Double-Strand Break Repair by Nonhomologous End Joining ScreenTroll: a searchable database to compare genome-wide yeast screens.DNA damage induces a meiotic arrest in mouse oocytes mediated by the spindle assembly checkpoint.Saccharomyces cerevisiae genetics predicts candidate therapeutic genetic interactions at the mammalian replication fork.Mutants defective in Rad1-Rad10-Slx4 exhibit a unique pattern of viability during mating-type switching in Saccharomyces cerevisiae.Drosophila myt1 is the major cdk1 inhibitory kinase for wing imaginal disc development.Centrosomal Che-1 protein is involved in the regulation of mitosis and DNA damage response by mediating pericentrin (PCNT)-dependent Chk1 protein localization The spindle assembly checkpoint: More than just keeping track of the spindle.Rad51-dependent aberrant chromosome structures at telomeres and ribosomal DNA activate the spindle assembly checkpoint.Similarities and differences between "uncapped" telomeres and DNA double-strand breaks.Microtubule attachment and spindle assembly checkpoint signalling at the kinetochore.Synthetic Physical Interactions Map Kinetochore-Checkpoint Activation Regions.EDD, a ubiquitin-protein ligase of the N-end rule pathway, associates with spindle assembly checkpoint components and regulates the mitotic response to nocodazole.Responding to chromosomal breakage during M-phase: insights from a cell-free system.A role for the spindle assembly checkpoint in the DNA damage response.A mitosis-sensing caspase activation platform? New insights into the PIDDosome.CAML loss causes anaphase failure and chromosome missegregation.An Inhibitor of PIDDosome Formation.RAD51 maintains chromosome integrity and mitochondrial distribution during porcine oocyte maturation in vitro.Mad2 prolongs DNA damage checkpoint arrest caused by a double-strand break via a centromere-dependent mechanism.Defective histone supply causes condensin-dependent chromatin alterations, SAC activation and chromosome decatenation impairment.DNA damage induces a kinetochore-based ATM/ATR-independent SAC arrest unique to the first meiotic division in mouse oocytes.Caenorhabditis elegans BUB-3 and SAN-1/MAD3 Spindle Assembly Checkpoint Components Are Required for Genome Stability in Response to Treatment with Ionizing Radiation.Function and regulation mechanism of Chk1 during meiotic maturation in porcine oocytes.

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P2860

DNA damage activates the SAC in an ATM/ATR-dependent manner, independently of the kinetochore.

http://www.wikidata.org/entity/Q30443388

description

2008 nî lūn-bûn

@nan

2008 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2008 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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DNA damage activates the SAC i ...... ependently of the kinetochore.

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DNA damage activates the SAC i ...... ependently of the kinetochore.

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JOURNAL.PGEN.1000015

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DNA damage activates the SAC i ...... ependently of the kinetochore.

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Daniel J Burke

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Eun Mi Kim

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P2860

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

Additional modules for versatile and economical PCR-based gene deletion and modification in Saccharomyces cerevisiae

APC(Cdc20) promotes exit from mitosis by destroying the anaphase inhibitor Pds1 and cyclin Clb5.

The Ipl1-Aurora protein kinase activates the spindle checkpoint by creating unattached kinetochores.

The centromeric protein Sgo1 is required to sense lack of tension on mitotic chromosomes.

MAD3 encodes a novel component of the spindle checkpoint which interacts with Bub3p, Cdc20p, and Mad2p.

Budding yeast Cdc20: a target of the spindle checkpoint.

A mitotic topoisomerase II checkpoint in budding yeast is required for genome stability but acts independently of Pds1/securin.

Recovery from DNA replicational stress is the essential function of the S-phase checkpoint pathway.

Cell cycle execution point analysis of ORC function and characterization of the checkpoint response to ORC inactivation in Saccharomyces cerevisiae.

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