Đang chuẩn bị liên kết để tải về tài liệu:
Báo cáo sinh học: "ERK2 mitogen-activated protein kinases affect Ras-dependent cell signaling differentially"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: ERK1 and ERK2 mitogen-activated protein kinases affect Ras-dependent cell signaling differentially. | J. Biol. Journal of Biology BioMed Central Research article Open Access ERKI and ERK2 mitogen-activated protein kinases affect Ras-dependent cell signaling differentially Chiara Vantaggiato 1 Ivan FormentinC Attilio Bondanza Chiara Bonini Luigi Naldini and Riccardo Brambilla Address Tstituto Scientifico San Raffaele and Università Vita-Salute San Raffaele Via Olgettina 58 20132 Milano Italy. Current address Istituto Scientifico E. Medea 23848 Bosisio Parini Italy. These authors equally contributed to this work. Correspondence Riccardo Brambilla. Email brambilla.riccardo@hsr.it Published 28 June 2006 Received II January 2005 Revised 17 February 2006 Journal of Biology 2006 5 14 J Igy Accepted 6 April 2006 The electronic version of this article is the complete one and can be found online at http jbiol.com content 5 5 14 2006 Vantaggiato and Formentini et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The mitogen-activated protein MAP kinases p44ERK1 and p42ERK2 are crucial components of the regulatory machinery underlying normal and malignant cell proliferation. A currently accepted model maintains that ERK1 and ERK2 are regulated similarly and contribute to intracellular signaling by phosphorylating a largely common subset of substrates both in the cytosol and in the nucleus. Results Here we show that ablation of ERK1 in mouse embryo fibroblasts and NIH 3T3 cells by gene targeting and RNA interference results in an enhancement of ERK2-dependent signaling and in a significant growth advantage. By contrast knockdown of ERK2 almost completely abolishes normal and Ras-dependent cell proliferation. Ectopic expression of ERK1 but not of ERK2 in NIH 3T3 cells inhibits oncogenic Ras-mediated proliferation .