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PMS1 postmeiotic segregation increased 1

This gene encodes a protein belonging to the DNA mismatch repair mutL/hexB family. This protein is thought to be involved in the repair of DNA mismatches, and it can form heterodimers with MLH1, a known DNA mismatch repair protein. Mutations in this gene cause hereditary nonpolyposis colorectal cancer type 3 (HNPCC3) either alone or in combination with mutations in other genes involved in the HNPCC phenotype, which is also known as Lynch syndrome. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MLH1, MSH2, PMS2, MSH6, CAN
Papers on PMS1
Identification of candidate genes associated with fertility restoration of cytoplasmic male-sterility in onion (Allium cepa L.) using a combination of bulked segregant analysis and RNA-seq.
Choi et al., Kwangju, South Korea. In Theor Appl Genet, Nov 2015
Among them, the gene encoding PMS1, involved in the DNA mismatch repair pathway, was assumed to be the best candidate gene responsible for fertility restoration of male-sterility in onion.
Segregation of a novel MLH1 mutation in an Iranian Lynch syndrome family.
Miryounesi et al., Tehrān, Iran. In Gene, Nov 2015
This mutation is located in a region coding for the functional domain for the interaction with MLH3/PMS1/PMS2.
MCM9 Is Required for Mammalian DNA Mismatch Repair.
Méchali et al., Montpellier, France. In Mol Cell, Oct 2015
Here, we show that mammalian MCM9, a protein involved in replication and homologous recombination, forms a complex with MMR initiation proteins (MSH2, MSH3, MLH1, PMS1, and the clamp loader RFC) and is essential for MMR.
A Genetic Incompatibility Accelerates Adaptation in Yeast.
Alani et al., Toronto, Canada. In Plos Genet, Jul 2015
During mismatch repair (MMR) MSH proteins bind to mismatches that form as the result of DNA replication errors and recruit MLH factors such as Mlh1-Pms1 to initiate excision and repair steps.
DNA mismatch repair enzymes: genetic defects and autoimmunity.
Akiyama et al., Nagoya, Japan. In Clin Chim Acta, Apr 2015
The human MutS enzymes consist of MSH2, MSH3 and MSH6, and the human MutL enzymes include MLH1, MLH3, PMS1 and PMS2.
Clinical and Molecular Characterization of Brazilian Patients Suspected to Have Lynch Syndrome.
Carraro et al., São Paulo, Brazil. In Plos One, 2014
Nowadays, LS is regarded of patients who carry deleterious germline mutations in one of the five mismatch repair genes (MMR), mostly in MLH1 and MSH2, but also in MSH6, PMS1 and PMS2.
Mismatch repair pathway: molecules, functions, and role in colorectal carcinogenesis.
Fatima et al., Srīnagar, India. In Eur J Cancer Prev, 2014
Mutations in at least five pivotal genes of MMR, namely, in those encoding mutS homolog 2 (MSH2), mutL homolog 1 (MLH1), mutS homolog 6 (MSH6), postmeiotic segregation increased 1 (PMS1), and postmeiotic segregation, increased 2 (PMS2) have been found in CRC, highlighting the importance of understanding the basic structure and functions of the essential molecules that make up the MMR system.
Mismatch repair deficiency in ovarian cancer -- molecular characteristics and clinical implications.
Gourley et al., Edinburgh, United Kingdom. In Gynecol Oncol, 2014
The incidence of germline MMR gene mutations in ovarian cancer is only 2% but other mechanisms of gene inactivation mean that loss of expression of one of the seven main genes (MSH2, MSH3, MSH6, MLH1, MLH3, PMS1 and PMS2) occurs in up to 29% of cases.
Hereditary breast and ovarian cancer susceptibility genes (review).
Matsuura et al., Kashihara, Japan. In Oncol Rep, 2013
Mutations in BRCA genes cannot account for all cases of HBOC, indicating that the remaining cases can be attributed to the involvement of constitutive epimutations or other cancer susceptibility genes, which include Fanconi anemia (FA) cluster (FANCD2, FANCA and FANCC), mismatch repair (MMR) cluster (MLH1, MSH2, PMS1, PMS2 and MSH6), DNA repair cluster (ATM, ATR and CHK1/2), and tumor suppressor cluster (TP53, SKT11 and PTEN).
Hereditary genes and SNPs associated with breast cancer.
Nasiri et al., Mashhad, Iran. In Asian Pac J Cancer Prev, 2012
The most important loci which include mutations are; BRCA1, BRCA2, PTEN, ATM, TP53, CHEK2, PPM1D, CDH1, MLH1, MRE11, MSH2, MSH6, MUTYH, NBN, PMS1, PMS2, BRIP1, RAD50, RAD51C, STK11 and BARD1.
The unstructured linker arms of Mlh1-Pms1 are important for interactions with DNA during mismatch repair.
Alani et al., Ithaca, United States. In J Mol Biol, 2012
The unstructured linker arms of Mlh1-Pms1 are important for interactions with DNA during mismatch repair
Functional residues on the surface of the N-terminal domain of yeast Pms1.
Kunkel et al., United States. In Dna Repair (amst), 2010
Functional residues on the surface of the N-terminal domain of yeast Pms1
Direct visualization of asymmetric adenine-nucleotide-induced conformational changes in MutL alpha.
Erie et al., Chapel Hill, United States. In Mol Cell, 2008
Adenine nucleotides induce large asymmetric conformational changes in full-length yeast MutL alpha. These changes are associated with significant increases in secondary structure.
Characterization of the interactome of the human MutL homologues MLH1, PMS1, and PMS2.
Jiricny et al., Zürich, Switzerland. In J Biol Chem, 2007
In pstreplicative mismatch repair, this protein interacts wiwth MutL protein.
Negative epistasis between natural variants of the Saccharomyces cerevisiae MLH1 and PMS1 genes results in a defect in mismatch repair.
Alani et al., Ithaca, United States. In Proc Natl Acad Sci U S A, 2006
Saccharomyces cerevisiae strains bearing the S288c-strain-derived MLH1 gene and the SK1-strain-derived PMS1 gene displayed elevated mutation rates that conferred a long-term fitness cost
MLH3: a DNA mismatch repair gene associated with mammalian microsatellite instability.
Collins et al., Bethesda, United States. In Nat Genet, 2000
Functional redundancy among Mlh3, Pms1 and Pms2 may explain why neither Pms1 nor Pms2 mutant mice develop colon cancer, and why PMS1 and PMS2 mutations are only rarely found in HNPCC families.
Meiotic instability of human minisatellite CEB1 in yeast requires DNA double-strand breaks.
Nicolas et al., Paris, France. In Nat Genet, 1999
Using mutations affecting the initiation of recombination (spo11) or mismatch repair (msh2 pms1 ), we demonstrate that meiotic destabilization depends on the initiation of homologous recombination at nearby DNA double-strand break (DSBs) sites and involves a 'rearranged heteroduplex' intermediate.
Involvement of nucleotide-excision repair in msh2 pms1-independent mismatch repair.
Kohli et al., Bern, Switzerland. In Nat Genet, 1999
In Schizosaccharomyces pombe, the msh2- and pms1-dependent long-patch MMR system efficiently corrects small insertion/deletion loops and all base-base mismatches, except C/C.
Clinical findings with implications for genetic testing in families with clustering of colorectal cancer.
Fodde et al., Leiden, Netherlands. In N Engl J Med, 1998
BACKGROUND: Germ-line mutations in DNA mismatch-repair genes (MSH2, MLH1, PMS1, PMS2, and MSH6) cause susceptibility to hereditary nonpolyposis colorectal cancer.
Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair.
Liskay et al., Houston, United States. In Nat Genet, 1998
Germline mutations in the human MSH2, MLH1, PMS2 and PMS1 DNA mismatch repair (MMR) gene homologues appear to be responsible for most cases of hereditary non-polyposis colorectal cancer (HNPCC; refs 1-5).
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