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Activation and signaling of the p38 MAP kinase pathway

Cell Research 2005年第1期15卷 11-18页

作者： tyler zarubin La Jolla USA Department of Immunology 10550 N. Torrey Pines Road The Scripps Research Institute CA 92037

The family members of the mitogen-activated protein (MAP) kinases mediate a wide variety of cellular behaviors in response to extracellular stimuli. One of the four main sub-groups, the p38 group of MAP kinases, serve as a nexus for signal transduction and play a vital role in numerous biological processes. In this review, we highlight the known characteristics and components of the p38 pathway along with the mechanism and consequences of p38 activation. We focus on the role of p38 as a signal transduction mediator and examine the evidence linking p38 to inflammation, cell cycle, cell death, development, cell differentiation, senescence and tumorigenesis in specific cell types. Upstream and downstream components of p38 are described and questions remaining to be answered are posed. Finally, we propose several directions for future research on p38.

关键词： p38 MAP kinase signaling pathway nexus inflammation differentiation senescence tumorigenesis.

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Identification of eight genes that are potentially involved in tamoxifen sensitivity in breast cancer cells

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Cell Research 2005年第6期15卷 439-446页

作者： tyler zarubin Department of Immunology The Scripps Research Institute 10550 North Torrey Pines Road La Jolla CA 92037 USA

Although the antiestrogen agent tamoxifen has long been used to treat women with hormone receptor positive inva-sive breast carcinoma, the mechanisms of its action and acquired resistance to tamoxifen during treatment are largelyunknown. A number of studies have revealed that over-activation of some signaling pathways can cause tamoxifenresistance; however, very little information is available regarding the genes whose loss-of-function alternation contrib-ute to tamoxifen resistance. Here we used a forward genetic approach in vitro to generate tamoxifen resistant cells fromthe tamoxifen sensitive breast cancer cell line ZR-75-1, and further identified the disrupted gene in different tamoxifenresistant clones. Retinol binding protein 7, DNA polymerase-transactivated protein 3, γ-glutamyltransferase-like activity 1,slit-robo RhoGTPase-activating protein, tetraspan NET-4, HSPC194, amiloride-sensitive epithelial sodium channel gene,and Notch2, were the eight mutated genes identified in different tamoxifen resistant clones, suggesting their requirementfor tamoxifen sensitivity in ZR-75-1 cells. Since the functions of these genes are not related to each other, it suggeststhat multiple pathways can influence tamoxifen sensitivity in breast cancer cells.

关键词： tamoxifen breast cancer gene identification.

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