The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase (Q28512554)

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English	The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase	scientific journal article

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scholarly article

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PubMed publication ID

25 January 2017

The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase (English)

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PubMed publication ID

25 January 2017

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GOA release 2020-03-11

MRE11A homolog A, double strand break repair nuclease

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GOA release 2020-03-11

DNA mismatch repair

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Annapaola Franchitto

object named as

Annapaola Franchitto

1

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Pietro Pichierri

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Pietro Pichierri

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Marco Crescenzi

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Marco Crescenzi

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author name string

Rita Piergentili

3

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PubMed publication ID

25 January 2017

Margherita Bignami

5

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PubMed publication ID

25 January 2017

Fabrizio Palitti

6

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PubMed publication ID

25 January 2017

language of work or name

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publication date

10 April 2003

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PubMed publication ID

25 January 2017

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PubMed publication ID

25 January 2017

22

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PubMed publication ID

25 January 2017

14

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PubMed publication ID

25 January 2017

2110–2120

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PubMed publication ID

25 January 2017

Targeting DNA mismatch repair for radiosensitization

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Increased somatic recombination in methylation tolerant human cells with defective DNA mismatch repair

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The Mre11 complex: at the crossroads of dna repair and checkpoint signalling

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21 January 2018

Mouse embryonic stem cells carrying one or two defective Msh2 alleles respond abnormally to oxidative stress inflicted by low-level radiation

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Genetic analysis of the DNA-dependent protein kinase reveals an inhibitory role of Ku in late S-G2 phase DNA double-strand break repair

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Mismatch repair defects in cancer

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BER, MGMT, and MMR in defense against alkylation-induced genotoxicity and apoptosis

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Eukaryotic DNA mismatch repair

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Homology-directed repair is a major double-strand break repair pathway in mammalian cells

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Sensing and responding to DNA damage.

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Mismatch repair in replication fidelity, genetic recombination, and cancer biology

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DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139

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Role of Saccharomyces cerevisiae Msh2 and Msh3 repair proteins in double-strand break-induced recombination

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Nuclease activities in a complex of human recombination and DNA repair factors Rad50, Mre11, and p95

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Mismatch repair, G(2)/M cell cycle arrest and lethality after DNA damage.

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Role of the human RAD51 protein in homologous recombination and double-stranded-break repair

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Functional interactions and signaling properties of mammalian DNA mismatch repair proteins

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Quantification of apoptotic cells with fluorescein isothiocyanate-labeled annexin V in chinese hamster ovary cell cultures treated with cisplatin

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X-ray induced DNA double strand break production and repair in mammalian cells as measured by neutral filter elution

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The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: linkage of double-strand break repair to the cellular DNA damage response

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Mismatch repair proteins regulate heteroduplex formation during mitotic recombination in yeast

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The mammalian mismatch repair pathway removes DNA 8-oxodGMP incorporated from the oxidized dNTP pool

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Mitotic crossovers between diverged sequences are regulated by mismatch repair proteins in Saccaromyces cerevisiae

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Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

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Repair of double-strand breaks by homologous recombination in mismatch repair-defective mammalian cells

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The Saccharomyces cerevisiae Msh2 mismatch repair protein localizes to recombination intermediates in vivo.

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Sensitivity to DNA cross-linking chemotherapeutic agents in mismatch repair-defective cells in vitro and in xenografts

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Caffeine effect on the mitotic delay induced by G2 treatment with UVC or mitomycin C.

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Cdc25 inhibited in vivo and in vitro by checkpoint kinases Cds1 and Chk1

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The many interfaces of Mre11

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DNA damage-induced activation of p53 by the checkpoint kinase Chk2

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Mismatch repair and differential sensitivity of mouse and human cells to methylating agents.

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Chemical changes induced in DNA by ionizing radiation.

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Eukaryotic mismatch repair: an update

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Molecular mechanisms of DNA double strand break repair

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DNA damage tolerance, mismatch repair and genome instability

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Biochemistry and genetics of eukaryotic mismatch repair

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hMre11 and hRad50 nuclear foci are induced during the normal cellular response to DNA double-strand breaks

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

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DNA damage-dependent nuclear dynamics of the Mre11 complex

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Chromosome radiosensitivity in human G2 lymphocytes and cell-cycle progression

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The 3' to 5' exonuclease activity of Mre 11 facilitates repair of DNA double-strand breaks

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A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage

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Hypersensitivity to camptothecin in MSH2 deficient cells is correlated with a role for MSH2 protein in recombinational repair

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Conservation of the Chk1 checkpoint pathway in mammals: linkage of DNA damage to Cdk regulation through Cdc25

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Classification and relationships of induced chromosomal structual changes

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Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death

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Homologous recombination and non-homologous end-joining pathways of DNA double-strand break repair have overlapping roles in the maintenance of chromosomal integrity in vertebrate cells

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Involvement of Brca1 in S-phase and G(2)-phase checkpoints after ionizing irradiation

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Two molecularly distinct G(2)/M checkpoints are induced by ionizing irradiation

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Mre11 is essential for the maintenance of chromosomal DNA in vertebrate cells

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Mismatch repair is required for O(6)-methylguanine-induced homologous recombination in human fibroblasts

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Association of p53 and MSH2 with recombinative repair complexes during S phase

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