Hmsh6
Mostrando 1-12 de 23 artigos, teses e dissertações.
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1. Expressão de marcadores imunoistoquímicos de origem tecidual e de carcinogênese nos adenocarcinomas tipo intestinal e pancreatobiliar da ampola de Vater / Immunohistochemistry expression of tissue origin and carcinogenesis markers in adenocarcinomas of intestinal and pancreaticobiliary types of Vaters ampolla
INTRODUÇÃO: Os adenocarcinomas da ampola de Vater (AAV) são classificados conforme a diferenciação histológica em tipos pancreatobliliar e intestinal, com comportamento biológico e prognóstico diferentes. O objetivo deste estudo foi determinar um painel imuno-histoquímico para a diferenciação do tipo histológico dos AAVs e analisar os fatores rel
Publicado em: 2009
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2. Study of immunohistochemical expressions of: hMLH1, hMSH2 and Cox-2 in colon polyps / Estudo imunohistoquímico das expressões: hMLH1, hMSH2 e Cox-2 em pólipos do cólon
Pólipos adenomatosos colorretais são conhecidos como lesões pré-malignas. Mutações germinativas nas enzimas de reparo (MMR) hMLH1, hMSH2 e hMSH6 são causas reconhecidas de câncer colorretal hereditário não polipóide, induzindo um fenótipo mutante caracterizado por instabilidade de microssatélite (MSI). A MSI também é detectada em cânceres col
Publicado em: 2007
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3. The presence of proteins hMLH1 and hMSH6 of DNA mismatch repair system in actinic cheilitis and squamous cell carcinoma of the lip / "A presença das proteínas hMLH1 e hMSH6 do sistema de reparo do mau pareamento do DNA em queilites actínicas e carcinomas epidermóides de lábio"
Actinic cheilitis (AC) results from chronic and excessive exposure of the lips to the ultraviolet radiation in sunlight. AC is recognized as a potentially malignant condition and it is estimated that 10% to 20% will become lip squamous cell carcinoma (LSCC). It has been suggested that virtually every LSCC was initially AC. It is well known that solar radiati
Publicado em: 2006
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4. Tumores gástricos primários múltiplos e únicos: análise imunohistoquímica comparativa / Multiple and solitary primary gastric tumors: comparative immunohistochemistry analysis
Introduction: Multiple primary gastric adenocarcinomas (MPGA) have been reported from 3.5% to 10% of all patients with gastric cancer. Tumoral multiplicity is largely known as an indicator of genetic predisposition for the development of neoplasias. Moreover, the route of carcinogenesis has not been clearly clarified in these tumors (mutator pathway or suppr
Publicado em: 2006
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5. hMSH2 forms specific mispair-binding complexes with hMSH3 and hMSH6
The genetic and biochemical properties of three human MutS homologues, hMSH2, hMSH3, and hMSH6, have been examined. The full-length hMSH6 cDNA and genomic locus were isolated and characterized, and it was demonstrated that the hMSH6 gene consisted of 10 exons and mapped to chromosome 2p15-16. The hMSH3 cDNA was in some cases found to contain a 27-bp del
The National Academy of Sciences of the USA.
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6. Interactions of Human hMSH2 with hMSH3 and hMSH2 with hMSH6: Examination of Mutations Found in Hereditary Nonpolyposis Colorectal Cancer
Mutations in the human mismatch repair protein hMSH2 have been found to cosegregate with hereditary nonpolyposis colorectal cancer (HNPCC). Previous biochemical and physical studies have shown that hMSH2 forms specific mispair binding complexes with hMSH3 and hMSH6. We have further characterized these protein interactions by mapping the contact regions withi
American Society for Microbiology.
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7. hMSH3 and hMSH6 interact with PCNA and colocalize with it to replication foci
Proliferating cell nuclear antigen (PCNA) has been implicated in eukaryotic postreplicative mismatch correction, but the nature of its interaction with the repair machinery remained enigmatic. We now show that PCNA binds to the human mismatch binding factors hMutSα and hMutSβ via their hMSH6 and hMSH3 subunits, respectively. The N-terminal domains of both
Cold Spring Harbor Laboratory Press.
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8. Functional analysis of human MutSalpha and MutSbeta complexes in yeast.
Mismatch repair (MMR) is initiated when a heterodimer of hMSH2*hMSH6 or hMSH2*hMSH3 binds to mismatches. Here we perform functional analyses of these human protein complexes in yeast. We use a sensitive genetic system wherein the rate of single-base deletions in a homopolymeric run in the LYS2 gene is 10 000-fold higher in an msh2 mutant than in a wild-type
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9. Functional characterization of two human MutY homolog (hMYH) missense mutations (R227W and V232F) that lie within the putative hMSH6 binding domain and are associated with hMYH polyposis
The base excision repair DNA glycosylase MutY homolog (MYH) is responsible for removing adenines misincorporated into DNA opposite guanine or 7,8-dihydro-8-oxo-guanine (8-oxoG), thereby preventing G:C to T:A mutations. Biallelic germline mutations in the human MYH gene predispose individuals to multiple colorectal adenomas and carcinoma. We have recently dem
Oxford University Press.
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10. Functional significance of concomitant inactivation of hMLH1 and hMSH6 in tumor cells of the microsatellite mutator phenotype
Genetic or epigenetic inactivation of one of the DNA mismatch repair (MMR) genes in tumor precursor cells causes a profound mutator phenotype, known as the microsatellite mutator phenotype (MMP). This mutator phenotype induces mutations not only in cancer genes that drive tumorigenesis but also in other DNA repair genes. The functional significance of t
The National Academy of Sciences.
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11. Interactions between p53, hMSH2–hMSH6 and HMG I(Y) on Holliday junctions and bulged bases
The ability of the tumor suppressor protein, p53, to recognize certain types of DNA lesions may represent one of the mechanisms by which this protein modulates cellular response to DNA damage. p53 DNA binding properties are regulated by several factors, such as post-translational modifications including phosphorylation and acetylation, regulation by its own
Oxford University Press.
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12. DHFR/MSH3 amplification in methotrexate-resistant cells alters the hMutSα/hMutSβ ratio and reduces the efficiency of base–base mismatch repair
The level and fate of hMSH3 (human MutS homolog 3) were examined in the promyelocytic leukemia cell line HL-60 and its methotrexate-resistant derivative HL-60R, which is drug resistant by virtue of an amplification event that spans the dihydrofolate reductase (DHFR) and MSH3 genes. Nuclear extracts from HL-60 and HL-60R cells were subjected to an identical,
The National Academy of Sciences of the USA.