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Id: lil-99487
Autor: Chauhan, M. A; Ali, M; Vedeckis, W. V; Salas, C. E.
Título: Transfer RNA nucleoside composition in 13762 rat adenocarcinoma
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;24(6):547-58, 1991. tab.
Idioma: en.
Resumo: Abnormalities in patterns of RNA methylation and in the activities of tRNA methyltransferases are well-documented phenomena. In this study, we focused our attention on tRNA from adenocarcinoma, a 9,10-dimethyl-1,2-benznthracene-induced mammary tumor, because prior evidence has suggested the occurence of an abnormal pattern of tRNA methylation. Chemical postlabeling of tumor vs normal rat liver and mammary gland tRNAs revealed tumor specific differences in the modified nucleoside distribution, i.e., a 5.8-fold increase in tumor n-2-methylguanosine together with a 2.7-,2.8-,2.6-, and 2.8-fold decrease in tumor 1-methyladenosine, dihydrouridine, pseudoridine and 5-methylcytidyne, respectively. Class A tRNAs, a slower gel migrating group of tumor tRNAs, exhibited even lower 1-methyladenosine levels. Most of the remaining nucleosides in class A tRNAs showed molar ratios similar to those found in bulk tumor tRNA. However, N-2-methylguanosine levels class A tRNA are intermediate between bulk tumor tRNA (2.8%) and mammary gland tRNA (0.49%). The only qualitative difference found in tumor tRNA seems to be the absence of inosine usually present in tRNAs from liver and mammary tissues. In spite of its abnormal methylation pattern adenocarcinoma tRNA binds to glucocorticoid receptor protein from mouse AtT-20 cells, generating a 65 tRNA-protein complex, in a fashion similar to that previously described for the endogenous tRNA isolated from the same cells
Descritores: Adenocarcinoma/enzimologia
Neoplasias Mamárias Experimentais/enzimologia
Nucleosídeos/análise
tRNA Metiltransferases/análise
-Composição de Bases
Fígado/enzimologia
Glândulas Mamárias Animais/enzimologia
Metilação
Ratos Endogâmicos F344
Limites: Animais
Feminino
Ratos
Tipo de Publ: Estudo Comparativo
Responsável: BR26.1 - Biblioteca Central



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