نتایج جستجو برای: msh2

تعداد نتایج: 1696  

2013
N. Cooley R. H. Elder A. C. Povey

The DNA mismatch repair (MMR) and base excision repair (BER) systems are important determinants of cellular toxicity following exposure to agents that cause oxidative DNA damage. To examine the interactions between these different repair systems, we examined whether toxicity, induced by t-BOOH and KBrO3, differs in BER proficient (Mpg (+/+), Nth1 (+/+)) and deficient (Mpg (-/-), Nth1 (-/-)) mou...

Journal: :Molecular cancer research : MCR 2014
Jun Aoi Motoyoshi Endo Tsuyoshi Kadomatsu Keishi Miyata Aki Ogata Haruki Horiguchi Haruki Odagiri Tetsuro Masuda Satoshi Fukushima Masatoshi Jinnin Satoshi Hirakawa Tomohiro Sawa Takaaki Akaike Hironobu Ihn Yuichi Oike

UNLABELLED Chronic inflammation has received much attention as a risk factor for carcinogenesis. We recently reported that Angiopoietin-like protein 2 (Angptl2) facilitates inflammatory carcinogenesis and metastasis in a chemically induced squamous cell carcinoma (SCC) of the skin mouse model. In particular, we demonstrated that Angptl2-induced inflammation enhanced susceptibility of skin tissu...

2013
Fernando Grigera Alfonso Bellacosa Amy L. Kenter

Mismatch repair (MMR) safeguards against genomic instability and is required for efficient Ig class switch recombination (CSR). Methyl CpG binding domain protein 4 (MBD4) binds to MutL homologue 1 (MLH1) and controls the post-transcriptional level of several MMR proteins, including MutS homologue 2 (MSH2). We show that in WT B cells activated for CSR, MBD4 is induced and interacts with MMR prot...

Journal: :Molecular and cellular biology 1999
B Studamire G Price N Sugawara J E Haber E Alani

Yeast Msh2p forms complexes with Msh3p and Msh6p to repair DNA mispairs that arise during DNA replication. In addition to their role in mismatch repair (MMR), the MSH2 and MSH3 gene products are required to remove 3' nonhomologous DNA tails during genetic recombination. The mismatch repair genes MSH6, MLH1, and PMS1, whose products interact with Msh2p, are not required in this process. We have ...

Journal: :Genetic testing 2005
Monika Grabowski Yvonne Mueller-Koch Eva Grasbon-Frodl Udo Koehler Gisela Keller Holger Vogelsang Wolfgang Dietmaier Reinhard Kopp Ulrike Siebers Wolfgang Schmitt Birgit Neitzel Maria Gruber Christa Doerner Brigitte Kerker Petra Ruemmele Gabriele Henke Elke Holinski-Feder

Hereditary nonpolyposis colorectal cancer (HNPCC) is due to defects in DNA mismatch repair (MMR) genes MSH2, MLH1, MSH6, and to a lesser extent PMS2. Of 466 suspected HNPCC families, we defined 54 index patients with either tumors of high microsatellite instability (MSI-H) and/or loss of expression for either MLH1, MSH2, and/or MSH6, but without a detectable pathogenic point mutation in these g...

2014
Christopher S. Campbell Hans Hombauer Anjana Srivatsan Nikki Bowen Kerstin Gries Arshad Desai Christopher D. Putnam Richard D. Kolodner

In Saccharomyces cerevisiae, the essential mismatch repair (MMR) endonuclease Mlh1-Pms1 forms foci promoted by Msh2-Msh6 or Msh2-Msh3 in response to mispaired bases. Here we analyzed the Mlh1-Mlh2 complex, whose role in MMR has been unclear. Mlh1-Mlh2 formed foci that often colocalized with and had a longer lifetime than Mlh1-Pms1 foci. Mlh1-Mlh2 foci were similar to Mlh1-Pms1 foci: they requir...

Journal: :The Journal of Cell Biology 2005
Nadine K. Kolas Anton Svetlanov Michelle L. Lenzi Frank P. Macaluso Steven M. Lipkin R. Michael Liskay John Greally Winfried Edelmann Paula E. Cohen

Mammalian MutL homologues function in DNA mismatch repair (MMR) after replication errors and in meiotic recombination. Both functions are initiated by a heterodimer of MutS homologues specific to either MMR (MSH2-MSH3 or MSH2-MSH6) or crossing over (MSH4-MSH5). Mutations of three of the four MutL homologues (Mlh1, Mlh3, and Pms2) result in meiotic defects. We show herein that two distinct compl...

Journal: :Cancer research 2015
José L McFaline-Figueroa Christian J Braun Monica Stanciu Zachary D Nagel Patrizia Mazzucato Dewakar Sangaraju Edvinas Cerniauskas Kelly Barford Amanda Vargas Yimin Chen Natalia Tretyakova Jacqueline A Lees Michael T Hemann Forest M White Leona D Samson

Glioblastoma (GBM) is often treated with the cytotoxic drug temozolomide, but the disease inevitably recurs in a drug-resistant form after initial treatment. Here, we report that in GBM cells, even a modest decrease in the mismatch repair (MMR) components MSH2 and MSH6 have profound effects on temozolomide sensitivity. RNAi-mediated attenuation of MSH2 and MSH6 showed that such modest decreases...

Journal: :Journal of medical genetics 2004
E Domingo P Laiho M Ollikainen M Pinto L Wang A J French J Westra T Frebourg E Espín M Armengol R Hamelin H Yamamoto R M W Hofstra R Seruca A Lindblom P Peltomäki S N Thibodeau L A Aaltonen S Schwartz

BACKGROUND According to the international criteria for hereditary non-polyposis colorectal cancer (HNPCC) diagnostics, cancer patients with a family history or early onset of colorectal tumours showing high microsatellite instability (MSI-H) should receive genetic counselling and be offered testing for germline mutations in DNA repair genes, mainly MLH1 and MSH2. Recently, an oncogenic V600E ho...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1997
N Sugawara F Pâques M Colaiácovo J E Haber

When gene conversion is initiated by a double-strand break (DSB), any nonhomologous DNA that may be present at the ends must be removed before new DNA synthesis can be initiated. In Saccharomyces cerevisiae, removal of nonhomologous ends depends not only on the nucleotide excision repair endonuclease Rad1/Rad10 but also on Msh2 and Msh3, two proteins that are required to correct mismatched bp. ...

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