QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?

Overriding MAP kinase

Transduction of extracellular signals that stimulate cell proliferation requires the small GTPase Ras. Precisely which Ras signalling pathways are involved remains obscure, however, given the numerous potential Ras effectors (e.g. Raf, PI3 kinase and phospholipase C) and doubts concerning the validity of the overexpression studies often used to define them. Chris Marshall and co-workers have now dissected mitogenic signalling through Ras by examining the requirement for ERK (part of the Ras-Raf-MEK-ERK MAP kinase cascade) signalling in cells lacking the tumour suppressor RB, using inhibitors of MEK to block ERK activation. Among their results is the observation that, unlike wild-type cells, RB^-/- mouse embryonic fibroblasts do not require significant ERK activation for exit from G0 phase and entry into S phase (see p. 4607). Since RB^-/- cells require Ras for exit from G0, this key finding indicates that although Ras/ERK signalling is required for the G1/S transition, an ERK-independent Ras mechanism drives exit from G0. It also demonstrates — for the first time — that loss of a tumour suppressor can alter cellular requirements for MAP kinase signalling.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

Related articles in JCS:

Loss of Rb overrides the requirement for ERK activity for cell proliferation

Giovanna M. D'Abaco, Steven Hooper, Hugh Paterson, and Christopher J. Marshall
JCS 2002 115: 4607-4616. [Abstract] [Full Text]  

This article has been cited by other articles:

				U. Korner, V. Fuss, J. Steigerwald, and H. Moll Biogenesis of Leishmania major-Harboring Vacuoles in Murine Dendritic Cells Infect. Immun., February 1, 2006; 74(2): 1305 - 1312. [Abstract] [Full Text] [PDF]

				A. G. Tempone, D. Perez, S. Rath, A. L. Vilarinho, R. A. Mortara, and H. F. de Andrade Jr Targeting Leishmania (L.) chagasi amastigotes through macrophage scavenger receptors: the use of drugs entrapped in liposomes containing phosphatidylserine J. Antimicrob. Chemother., July 1, 2004; 54(1): 60 - 68. [Abstract] [Full Text] [PDF]

				A. Shiratsuchi, I. Watanabe, O. Takeuchi, S. Akira, and Y. Nakanishi Inhibitory Effect of Toll-Like Receptor 4 on Fusion between Phagosomes and Endosomes/Lysosomes in Macrophages J. Immunol., February 15, 2004; 172(4): 2039 - 2047. [Abstract] [Full Text] [PDF]

				E. Prina, S. Z. Abdi, M. Lebastard, E. Perret, N. Winter, and J.-C. Antoine Dendritic cells as host cells for the promastigote and amastigote stages of Leishmania amazonensis: the role of opsonins in parasite uptake and dendritic cell maturation J. Cell Sci., January 15, 2004; 117(2): 315 - 325. [Abstract] [Full Text] [PDF]

				J. A. Schwarz and V. M. Weis Localization of a Symbiosis-Related Protein, Sym32, in the Anthopleura elegantissima-Symbiodinium muscatinei Association Biol. Bull., December 1, 2003; 205(3): 339 - 350. [Abstract] [Full Text] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?