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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Oncobiología > DA - CIMA - Terapia génica y Hepatología - Oncobiología - Artículos de revista >

S-adenosylmethionine regulates MAT1A and MAT2A gene expression in cultured rat hepatocytes: a new role for S-adenosylmethionine in the maintenance of the differentiated status of the liver
Authors: Garcia-Trevijano, E.R. (Elena R.)
Latasa, M.U. (María Ujué)
Carretero, M.V. (M. Victoria)
Berasain, C. (Carmen)
Mato, J.M. (José María)
Avila, M.A. (Matías Antonio)
Keywords: Biological methylation
Hepatocarcinoma
Methionine metabolism
Gene expression
Issue Date: 2000
Publisher: Federation of American Society of Experimental Biology
Publisher version: http://www.fasebj.org/content/14/15/2511
ISSN: 1530-6860
Citation: Garcia-Trevijano ER, Latasa MU, Carretero MV, Berasain C, Mato JM, Avila MA. S-adenosylmethionine regulates MAT1A and MAT2A gene expression in cultured rat hepatocytes: a new role for S-adenosylmethionine in the maintenance of the differentiated status of the liver. FASEB J 2000 Dec;14(15):2511-2518.
Abstract
Methionine metabolism starts with the formation of S-adenosylmethionine (AdoMet), the most important biological methyl donor. This reaction is catalyzed by methionine adenosyltransferase (MAT). MAT is the product of two different genes: MAT1A, which is expressed only in the adult liver, and MAT2A, which is widely distributed, expressed in the fetal liver, and replaces MAT1A in hepatocarcinoma. In the liver, preservation of high expression of MAT1A and low expression of MAT2A is critical for the maintenance of a functional and differentiated organ. Here we describe that in cultured rat hepatocytes MAT1A expression progressively decreased, as described for other liver-specific genes, and MAT2A expression was induced. We find that this switch in gene expression was prevented by adding AdoMet to the culture medium. We also show that in cultured hepatocytes with decreased MAT1A expression AdoMet addition markedly increased MAT1A transcription in a dose-dependent fashion. This effect of AdoMet was mimicked by methionine, and blocked by 3-deazaadenosine and L-ethionine, but not D-ethionine, indicating that the effect was specific and mediated probably by a methylation reaction. These findings identify AdoMet as a key molecule that differentially regulates MAT1A and MAT2A expression and helps to maintain the differentiated status of the hepatocyte.
Permanent link: http://hdl.handle.net/10171/23315
Appears in Collections:DA - CIMA - Terapia génica y Hepatología - Oncobiología - Artículos de revista

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