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* State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, People’s Republic of China; Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, 1333 San Pablo Street, Los Angeles, California 90033; and Department of Molecular Biology and Biochemistry, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, California 90089
To whom requests for reprints should be addressed at 1 Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, 1333 San Pablo Street (BMT-403), Los Angeles, CA 90033. E-mail: sying{at}hsc.usc.edu
Activins, cytokine members of the transforming growth factor-ß superfamily, have various effects on many physiological processes, including cell proliferation, cell death, metabolism, homeostasis, differentiation, immune responses endocrine function, etc. Activins interact with two structurally related serine/threonine kinase receptors, type I and type II, and initiate downstream signaling via Smads to regulate gene expression. Understanding how activin signaling is controlled extracellularly and intracellularly would not only lead to more complete understanding of cell growth and apoptosis, but would also provide the basis for therapeutic strategies to treat cancer and other related diseases. This review focuses on the recent progress on activin-receptor interactions, regulations of activin signaling by ligand-binding proteins, receptor-binding proteins, and nucleocytoplasmic shuttling of Smad proteins.
Key Words: activin • activin receptors • Smad • activin-binding protein • signaling pathway • cell proliferation • apoptosis • carcinogenesis • Cripto • betaglycan
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