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Welcome to the home for cell signaling information

The UCSD-Nature Signaling Gateway is a comprehensive and up-to-the-minute resource for anyone interested in signal transduction. This Gateway represents a unique collaboration between the University of California San Diego (UCSD) and Nature Publishing Group and is designed to facilitate navigation of the complex world of research into cellular signaling. Information and data presented here are freely available to all. It is powered by the San Diego Supercomputer Center (SDSC).

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cell signaling update

Last updated: 3 July 2008
Signaling Update brings you the latest cell signaling research, including primary research and reviews, news, jobs and conferences. more

cell signaling molecule pages

A database of key facts about the proteins involved in cell signaling, now covering well over 3,000 different proteins. more

10 MOST RECENTLY PUBLISHED: expert-authored, peer-reviewed information on: S6K1, S6K2, Phosphatidylinositol 4-kinase type II alpha, Gab1, Rcan1-4, AP-3 beta3a, AP-3 delta, Pink1, GABA A receptor alpha 6 subunit, AP-3 mu1.

View all published Molecule Pages

10 MOST POPULAR PAGES (June 2008): Calcium-sensing receptor, Catenin, beta, Pink1, GABA A receptor alpha 6 subunit, Gab1, Rac2, Luteinizing hormone receptor, Vav2, Rab8a, Wee1.

MOLECULE PAGE STATISTICS

Molecule Pages currently being prepared by authors287
Molecule Pages currently undergoing review107
Molecule Pages published448
data center

Archived primary research results from experiments previously performed by the Alliance for Cellular Signaling (AfCS), including B-lymphocyte and RAW 264.7 ligand screens and yeast two-hybrid data. more

about us

News and information about the San Diego Supercomputer Center (SDSC) and Nature Publishing Group (NPG). more

The Signaling Gateway has won the Association of Learned and Professional Society Publishers (ALPSP) Award for Publishing Innovation. This international award is presented annually to products that display ‘a significantly innovative approach to any aspect of publication’. more

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