C Ki Ras
Mostrando 1-12 de 96 artigos, teses e dissertações.
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1. The role of micro RNAs let7c, 100 and 218 expression and their target RAS, C-MYC, BUB1, RB, SMARCA5, LAMB3 and Ki-67 in prostate cancer
OBJECTIVE: The aim of this study is to verify the expression of proteins that are controlled by miR-let7c, 100 and 218 using immunohistochemistry in tissue microarray representative of localized and metastasized the lymph nodes and bone prostate cancer. METHODS: To verify the expression of proteins that are controlled by miR-let7c (C-MYC, BUB1, RAS) 100 (
Clinics. Publicado em: 2013-05
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2. Análise de proteínas cuja expressão é controlada por miRNA e relacionada à progressão do adenocarcinoma de próstata por imuno-histoquimica em tissue microarray / Analysis of proteins whose expression is controlled by miRNA and related to the progression of prostate adenocarcinoma by immunohistochemistry on tissue microarray
Introdução: O Câncer de Próstata (CaP) é o tumor mais comum do homem e a segunda causa de óbito por câncer no Brasil. MicroRNA (miRNA) é uma classe de pequenos RNA regulatórios não codificantes de proteínas que tem papel fundamental no controle da expressão dos genes. São responsáveis pelo controle de processos fundamentais na célula e estão
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 24/10/2012
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3. c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line
A linhagem tumoral Y1, originada de adrenocórtex decamundongo responde a FGF2 (Fator de Crescimento de Fibroblasto), possui o proto-oncogene c-ki-ras amplificado e a proteína c-Ki-Ras super-expressa e ativa (c-Ki-Ras-GTP). Em trabalhos anteriores mostramos que esta lesão genética causa ativação constitutiva da via de sinalização: c-Ki-Ras-GTP->PI3K->
Anais da Academia Brasileira de Ciências. Publicado em: 2006-06
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4. Immunohistochemical study of the molecular alterations in the astrocytic tumors: tumorigenic pathways and resistance markers / Estudo imuno-histoquímico das alterações moleculares nos tumores astrocíticos: vias tumorigênicas e indicadores de resistência
O presente estudo objetivou avaliar a expressão de genes envolvidos no processo tumorigênico e nos mecanismos de quimiorresistência dos tumores astrocíticos. Procedeu-se análise clínico-epidemiológica, avaliação histopatológica e estudo imuno-histoquímico das proteínas Ki-67, c-Myc, GFAP, p53, p21WAF1/CIP1, p27KIP1, Bcl-2, Bax, EGFR, erbB-2, p21R
Publicado em: 2005
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5. Human genome contains four genes homologous to transforming genes of Harvey and Kirsten murine sarcoma viruses.
Harvey and Kirsten murine sarcoma viruses each encode a structurally and functionally related 21-kilodalton protein (p21), which is the transforming protein of each virus. Using probes from the 0.9-kilobase (kb) p21-coding region of each virus (called v-Ha-ras and v-Ki-ras, respectively), we have molecularly cloned from normal human genomic DNA the sequences
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6. Identification of an activated c-Ki-ras oncogene in rat liver tumors induced by aflatoxin B1.
Weanling male Fischer rats were administered 40 intraperitoneal injections of aflatoxin B1 (25 micrograms per animal per day) over a 2-month period. This chronic dosing regimen resulted in the sequential formation of hyperplastic foci, preneoplastic nodules, and hepatocellular carcinomas in all of the animals treated. The presence of transforming DNA sequenc
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7. Chromosome assignments of four mouse cellular homologs of sarcoma and leukemia virus oncogenes.
Molecular probes for the oncogenes of Rous sarcoma virus (v-src), avian myeloblastosis virus (v-myb), Kirsten murine sarcoma virus (v-Ki-ras), and Harvey murine sarcoma virus (v-Ha-ras) were hybridized to the DNA from mouse-Chinese hamster somatic cell hybrids. The v-src, v-myb, v-Ki-ras, and v-Ha-ras genes each detected one or a few homologous mouse DNA fra
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8. Parental bias of Ki-ras oncogenes detected in lung tumors from mouse hybrids.
A mouse strain with low lung tumor susceptibility (C3H) and a strain with high lung tumor susceptibility (A/J) were reciprocally crossed to produce C3A and AC3 F1 hybrid mice. Ki-ras oncogenes were detected in spontaneous and chemically induced lung tumors obtained from the C3A and AC3 mice. To further explore the genetics of the Ki-ras gene in mouse lung tu
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9. Transcriptional activation of cKi-ras proto-oncogene resulting from retroviral promoter insertion.
Enhanced expression of the cKi-ras proto-oncogene in a bone marrow-derived mouse cell line, 416B, has been shown to be associated with the integration of Friend viral DNA into the cellular gene. Here we report the results of experiments designed to clarify the molecular mechanism responsible for the cKi-ras overexpression. Based on primer extension analyses
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10. Structure of the c-Ki-ras gene in a rat fibrosarcoma induced by 1,8-dinitropyrene.
Restriction enzyme maps were made of the region around exons 1 and 2 of activated c-Ki-ras of a fibrosarcoma (1,8-DNP2) induced in a rat by 1,8-dinitropyrene. Nucleotide sequence analysis revealed that activated c-Ki-ras shows a G----T transversion in codon 12 and consequently encodes cysteine instead of glycine in normal rat c-Ki-ras.
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11. Ovarian expression of cellular Ki-ras p21 varies with physiological status.
To elucidate the potential role of the ras protooncogene proteins in a specific tissue, the present study determined the levels of individual c-ras-encoded p21 proteins in the rat ovary during various stages of physiological function. p21 protein was extracted from ovaries taken from immature normal female rats, mature nonpregnant animals in the metestrus st
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12. Amplified DNA in Y1 mouse adrenal tumor cells: isolation of cDNAs complementary to an amplified c-Ki-ras gene and localization of homologous sequences to mouse chromosome 6.
We have isolated cDNA clones complementary to a c-Ki-ras cellular oncogene that is amplified in Y1 mouse adrenal tumor cells, with the amplified sequences located on double-minute chromatin bodies (DMs) and homogeneously staining chromosomal regions (HSRs). Characterization of the cDNAs included the isolation of corresponding genomic clones, Northern blot an