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The EMBO Journal, ISSN 0261-4189, 08/2014, Volume 33, Issue 15, pp. 1698 - 1712
Several proteins in the BRCA‐Fanconi anemia (FA) pathway, such as FANCJ, BRCA1, and FANCD2, interact with mismatch repair (MMR... 
mismatch repair | replication stress | FANCJ | Fanconi anemia | MLH1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-CELLS | DRUG-RESISTANCE | HUMAN MUTS | CELL BIOLOGY | CISPLATIN | STALLED REPLICATION FORKS | HOMOLOGOUS RECOMBINATION | G-QUADRUPLEX DNA | LINK REPAIR | HELICASE | POLYMERASE-ZETA | MutL Protein Homolog 1 | Basic-Leucine Zipper Transcription Factors - metabolism | Fanconi Anemia Complementation Group D2 Protein - genetics | Humans | MutS Homolog 2 Protein - metabolism | Fanconi Anemia Complementation Group A Protein - genetics | Fanconi Anemia Complementation Group A Protein - metabolism | DNA-Binding Proteins - metabolism | Cell Line - drug effects | Fanconi Anemia Complementation Group Proteins - metabolism | Mice, Mutant Strains | BRCA1 Protein - metabolism | DNA Mismatch Repair | Nuclear Proteins - genetics | DNA Damage - drug effects | Fanconi Anemia Complementation Group Proteins - genetics | DNA Replication | Nuclear Proteins - metabolism | MutS Homolog 2 Protein - genetics | Basic-Leucine Zipper Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mitomycin - pharmacology | Ubiquitin-Protein Ligases | BRCA1 Protein - genetics | Animals | Fanconi Anemia Complementation Group D2 Protein - metabolism | Adaptor Proteins, Signal Transducing - genetics | Chromosome Aberrations | Mice | Adaptor Proteins, Signal Transducing - metabolism | Proteins | DNA repair | DNA damage | Deoxyribonucleic acid--DNA | Cell cycle | Index Medicus
Journal Article
Cancer, ISSN 0008-543X, 2017, Volume 123, Issue 20, pp. 3925 - 3932
... protein Hox‐B13 ( HOXB13 ) gene on chromosome 17 through linkage analysis. The HOXB13 G84E mutation typically occurs on a common haplotype consistent with a founder... 
prostate cancer | germline variants | multiple primary malignant neoplasms | genetic testing | gene panel | GENOMICS | ONCOLOGY | COLORECTAL-CANCER | DNA | HOXB13 G84E MUTATION | RISK | LYNCH SYNDROME | Humans | Middle Aged | Male | Mutation, Missense | Checkpoint Kinase 2 - genetics | Prostatic Neoplasms - genetics | DNA Mutational Analysis | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Germ-Line Mutation | Adult | RNA Helicases - genetics | Neoplastic Syndromes, Hereditary - genetics | Neoplasms, Second Primary - genetics | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Genetic Predisposition to Disease | Neoplastic Syndromes, Hereditary - diagnosis | DNA-Binding Proteins - genetics | Fanconi Anemia Complementation Group Proteins | Sequence Analysis, DNA | Homeodomain Proteins - genetics | MutL Protein Homolog 1 - genetics | Age of Onset | Aged | Ataxia Telangiectasia Mutated Proteins - genetics | BRCA2 Protein - genetics | Care and treatment | Genetic aspects | Research | Gene mutations | Genetic variation | Prostate cancer | Fibroblast growth factor | Genes | DNA damage | Homology | Malignancy | Criteria | DNA repair | Genetic screening | Homeobox | DNA helicase | Proteins | Ataxia | Genetics | Deoxyribonucleic acid--DNA | Fibroblast growth factor receptor 3 | BRCA2 protein | CHK2 protein | Nucleotide sequence | BRCA1 protein | MLH1 protein | Health risks | Protein C | Breast cancer | Medical screening | Patients | Medical prognosis | Men | Ataxia telangiectasia mutated protein | Mutation | Prostate | Cancer | Fibroblast growth factor receptors
Journal Article
Genes, Chromosomes and Cancer, ISSN 1045-2257, 11/2017, Volume 56, Issue 11, pp. 769 - 787
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 11, p. e14060
... from excising the aberrant gemcitabine nucleotide [4], [5]. Incorporated gemcitabine can be recognized by p53 and DNA dependent protein kinase, which may induce apoptosis... 
EXCISION-REPAIR | METHYLATION | MECHANISM | CISPLATIN | HUMAN-CELLS | BIOLOGY | MISMATCH REPAIR | DRUG-RESISTANCE | CANCER | DAMAGE | 2',2'-DIFLUORODEOXYCYTIDINE | Xenopus | MutL Protein Homolog 1 | Xenopus Proteins - genetics | Humans | Deoxycytidine - pharmacology | HEK293 Cells | Cell Cycle Proteins - genetics | Oocytes - drug effects | Antimetabolites, Antineoplastic - pharmacology | Female | Epigenesis, Genetic - drug effects | Nuclear Proteins - genetics | DNA Repair - drug effects | Oocytes - metabolism | HCT116 Cells | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Gene Expression Regulation - drug effects | Animals | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Xenopus Proteins - metabolism | Adaptor Proteins, Signal Transducing - metabolism | DNA Methylation - drug effects | Deoxycytidine - analogs & derivatives | Epigenetic inheritance | Care and treatment | Gemcitabine | Analysis | Genes | DNA | Genetic engineering | Methylation | Health aspects | DNA repair | Cells | Cancer | Camptothecin | Leukemia | Oct-4 protein | Cytotoxicity | Kinases | Drug resistance | Cancer therapies | Base excision repair | Neurogenesis | Oocytes | Mammalian cells | Proteins | Demethylation | Embryology | Reporter gene | DNA methylation | Inhibition | Repair | Deoxyribonucleic acid--DNA | Enzymes | MLH1 protein | DNA topoisomerase | Polymerization | Nucleotide excision repair | DNA biosynthesis | Gene silencing | Chemotherapy | Gadd45A protein | Plasmids | Epigenetics | GADD45 protein | Tumors | Deoxyribonucleic acid
Journal Article
Human Pathology, ISSN 0046-8177, 2014, Volume 45, Issue 10, pp. 2029 - 2036
Summary Immunohistochemistry (IHC) testing for mismatch repair proteins (MMRP) is currently being used primarily in colorectal cancer resection specimens... 
Pathology | Lynch | HNPCC | Neoadjuvant | Immunohistochemical staining | Reliability | Chemoradiation | LYNCH-SYNDROME | PREMM1,2,6 | MICROSATELLITE INSTABILITY | GUIDELINES | RISK | PATHOLOGY | IDENTIFICATION | MLH1 | COLORECTAL-CANCER PATIENTS | MUTATIONS | MutL Protein Homolog 1 | Nuclear Proteins - analysis | Colorectal Neoplasms - genetics | Humans | Middle Aged | Adenosine Triphosphatases - drug effects | DNA-Binding Proteins - analysis | Male | Chemoradiotherapy | Immunohistochemistry - standards | DNA Repair Enzymes - radiation effects | Neoplasm Proteins - drug effects | Colorectal Neoplasms - therapy | Adenosine Triphosphatases - analysis | DNA Mismatch Repair | Female | MutS Homolog 2 Protein - radiation effects | Neoadjuvant Therapy | Mismatch Repair Endonuclease PMS2 | Nuclear Proteins - drug effects | Reproducibility of Results | DNA-Binding Proteins - radiation effects | MutS Homolog 2 Protein - drug effects | DNA-Binding Proteins - drug effects | Nuclear Proteins - radiation effects | Adaptor Proteins, Signal Transducing - radiation effects | DNA Repair Enzymes - analysis | Adaptor Proteins, Signal Transducing - analysis | Neoplasm Proteins - radiation effects | Neoplasm Proteins - analysis | Aged | MutS Homolog 2 Protein - analysis | Adaptor Proteins, Signal Transducing - drug effects | Adenosine Triphosphatases - radiation effects | DNA Repair Enzymes - drug effects | Proteins | Immunohistochemistry | DNA | Colorectal cancer | Cancer therapies | Surgery | Cloning | Deoxyribonucleic acid--DNA
Journal Article
Familial Cancer, ISSN 1389-9600, 4/2018, Volume 17, Issue 2, pp. 225 - 228
.... MMR protein immunohistochemistry (IHC) is currently widely used for the detection of MMR deficiency in solid tumors... 
Human Genetics | Biomedicine, general | Biomedicine | MLH1 methylation | MMR immunohistochemistry | Cancer Research | Microsatellite instability | Epidemiology | Double somatic mutation | Next generation sequencing | Lynch syndrome | ONCOLOGY | COLORECTAL-CANCER | GENETICS & HEREDITY | RISK | DEFICIENCY | Immunohistochemistry | Colonic Neoplasms - genetics | Adenocarcinoma - pathology | Humans | Gene Expression Regulation, Neoplastic | DNA-Binding Proteins - analysis | DNA Mismatch Repair - genetics | MutS Homolog 2 Protein - metabolism | DNA-Binding Proteins - metabolism | DNA Methylation | Mismatch Repair Endonuclease PMS2 - metabolism | Aged, 80 and over | Biomarkers, Tumor - metabolism | Germ-Line Mutation | Female | Adenocarcinoma - genetics | Biomarkers, Tumor - analysis | Mismatch Repair Endonuclease PMS2 - analysis | MutS Homolog 2 Protein - genetics | DNA-Binding Proteins - genetics | MutL Protein Homolog 1 - analysis | Phenotype | Colonic Neoplasms - pathology | MutL Protein Homolog 1 - genetics | Biomarkers, Tumor - genetics | MutL Protein Homolog 1 - metabolism | MutS Homolog 2 Protein - analysis | Mismatch Repair Endonuclease PMS2 - genetics | Proteins | Medical research | Colon cancer | Medicine, Experimental | Genetic aspects | Shiites | Methylation | Cancer | Adenocarcinoma | Phenotypes | MLH1 protein | MSH2 protein | Case reports | DNA repair | Carcinogenesis | MSH6 protein | MMR protein | Mismatch repair | Mutation | Solid tumors
Journal Article
Human Mutation, ISSN 1059-7794, 08/2010, Volume 31, Issue 8, pp. 975 - 982
... of MLH1/MSH2 missense variants with multivariate analysis of protein polymorphisms‐mismatch repair (MAPP‐MMR) . Hum Mutat 29 : 852 – 860 . Chen‐Shtoyerman R , Theodor... 
HNPCC | MutL | dimerization | PMS2 | MLH1 | missense mutation | Lynch syndrome | Missense mutation | Dimerization | MISSENSE VARIANTS | NONPOLYPOSIS COLORECTAL-CANCER | HUMAN MLH1 | HMUTS-ALPHA | PROTEIN-PROTEIN INTERFACES | COLON-CANCER | YEAST | GENETICS & HEREDITY | FUNCTIONAL-ANALYSIS | HUMAN MUTL-ALPHA | C-TERMINAL DOMAIN | Adaptor Proteins, Signal Transducing - chemistry | MutL Protein Homolog 1 | Immunoprecipitation | Humans | DNA Repair Enzymes - genetics | DNA Mismatch Repair - genetics | DNA-Binding Proteins - metabolism | DNA Repair Enzymes - metabolism | Protein Multimerization - genetics | Mismatch Repair Endonuclease PMS2 | Nuclear Proteins - genetics | DNA Repair Enzymes - chemistry | Protein Structure, Tertiary | Cell Line | Colorectal Neoplasms, Hereditary Nonpolyposis - genetics | Mutant Proteins - genetics | Adenosine Triphosphatases - metabolism | Models, Molecular | Mutant Proteins - metabolism | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Mutation - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Mutant Proteins - chemistry | Adaptor Proteins, Signal Transducing - genetics | Adenosine Triphosphatases - chemistry | Amino Acid Substitution - genetics | Adenosine Triphosphatases - genetics | Adaptor Proteins, Signal Transducing - metabolism | Cancer
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 12/2009, Volume 106, Issue 52, pp. 22223 - 22228
Escherichia coli MutS forms a mispair-dependent ternary complex with MutL that is essential for initiating mismatch repair (MMR) but is structurally... 
Proteins | Solvents | Biosensing techniques | DNA | Escherichia coli | Alleles | Amino acids | Genetic mutation | Saccharomyces cerevisiae | DNA mismatch repair | Mlh1-Pms1 | Msh2-Msh6 | Deuterium exchange | Mass spectrometry | Mismatch repair | EXCHANGE MASS-SPECTROMETRY | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | SACCHAROMYCES-CEREVISIAE MSH2-MSH6 | mismatch repair | deuterium exchange | DNA MISMATCH REPAIR | ESCHERICHIA-COLI MUTS | ATP HYDROLYSIS | DOMINANT MUTATIONS | mass spectrometry | PROTEIN COMPLEXES | BINDING | GENE-PRODUCT | MutS DNA Mismatch-Binding Protein - chemistry | DNA, Bacterial - metabolism | MutS DNA Mismatch-Binding Protein - metabolism | MutL Proteins | DNA, Bacterial - chemistry | Mannose-Binding Lectin - genetics | Recombinant Fusion Proteins - metabolism | Adenosine Triphosphate - metabolism | DNA Mismatch Repair | Escherichia coli - metabolism | MutS DNA Mismatch-Binding Protein - genetics | Protein Interaction Domains and Motifs | Mutagenesis, Site-Directed | Adenosine Triphosphatases - metabolism | Models, Molecular | Escherichia coli Proteins - metabolism | Recombinant Fusion Proteins - chemistry | Mannose-Binding Lectin - metabolism | DNA, Bacterial - genetics | Escherichia coli - genetics | Mannose-Binding Lectin - chemistry | Escherichia coli Proteins - genetics | Recombinant Fusion Proteins - genetics | Adenosine Triphosphatases - chemistry | Protein Conformation | Adenosine Triphosphatases - genetics | Escherichia coli Proteins - chemistry | Amino Acid Substitution | Mechanical properties | Usage | Biochemistry | Research | Binding proteins | Data processing | Mass spectroscopy | Hydrogen | ATP | MSH2 protein | Msh2–Msh6 | Biological Sciences | Mlh1–Pms1
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 6, p. e100523
Background: Friedreich ataxia (FRDA), the most common autosomal recessive ataxia disorder, is caused by a dynamic GAA repeat expansion mutation within intron 1... 
PARENTAL GENDER | DNA MISMATCH REPAIR | FRATAXIN | INSTABILITY | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | EXPANSION | STICKY DNA | GAA TRIPLET-REPEAT | MISSENSE MUTATIONS | RNA-POLYMERASE | Genomic Instability | MutL Protein Homolog 1 | Friedreich Ataxia - pathology | Humans | MutL Proteins | DNA Repair Enzymes - genetics | DNA-Binding Proteins - deficiency | Friedreich Ataxia - genetics | DNA-Binding Proteins - metabolism | DNA Mismatch Repair | Nuclear Proteins - deficiency | DNA Repair Enzymes - metabolism | Transcription, Genetic | Mismatch Repair Endonuclease PMS2 | Nuclear Proteins - genetics | Dimerization | DNA Repair Enzymes - chemistry | DNA Repair Enzymes - deficiency | Adenosine Triphosphatases - deficiency | Cell Line | Friedreich Ataxia - metabolism | HCT116 Cells | Mice, Inbred C57BL | Adenosine Triphosphatases - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Trinucleotide Repeat Expansion | Mice, Knockout | Phenotype | Animals | Adaptor Proteins, Signal Transducing - deficiency | Adaptor Proteins, Signal Transducing - genetics | Iron-Binding Proteins - genetics | Adenosine Triphosphatases - genetics | Mice | Adaptor Proteins, Signal Transducing - metabolism | Cell culture | Health sciences | Animal models | Yeast | Disease | Transcription | Gene regulation | Proteins | MSH6 protein | Frataxin | Transgenic animals | Mismatch repair | Rodents | Ataxia | Deoxyribonucleic acid--DNA | Medical research | Enzymes | Stability | MLH1 protein | Transgenic mice | MSH2 protein | Stability analysis | RNA polymerase | Gene expression | Hereditary diseases | Friedreich's ataxia | Stem cells | Mutation | Genetic recombination | Cancer | Deoxyribonucleic acid | DNA
Journal Article