Controlling TGF-beta signaling
Article Abstract:
Control of transforming growth factor beta (TGF-beta) signaling, the pathways of which have equally important extra- and intracellular phases, is discussed in this review article. Regulation mechanisms in the prereceptor phase of a TGF-beta signaling pathway can be as complicated and as important physiologically as those downstream of the receptors for TGF-beta.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2000
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Neurotrophins: key regulators of cell fate and cell shape in the vertebrate nervous system
Article Abstract:
Neurotrophins, key regulators of cell shapes and cell fates in the nervous system of vertebrates, are discussed in this review article. A two-receptor system is used for neurotrophin signaling, and neuroprophin receptor expression is highly regulated. The neurotrophins control survival of neurons in that they prevent and cause programmed cell death. They also regulate growth of neuronal processes. Topics include signal transduction through the Trk receptors, the splice variants of these receptors, signal transduction through the neurotrophin receptor p75, variants of the p75 receptor, nuclear targets of neurotrophin signaling, and neurotrophins and synaptic transmission.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2000
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Crystal structure of the cytoplasmic domain of the type I TGFbeta receptor in complex with FKBP12
Article Abstract:
The crystal structure of a fragment of an unphosphorylated type I TGFbeta receptor (TbetaR-I), which contains the GS region and catalytic domain, was investigated in complex with the FKBP12 binding protein. The TbetaR-I was found to adopt an inactive conformation that is maintained by the unphosphorylated GS region and further stabilized by the binding of the FKBP12 to the GS region of the receptor. Results also showed that certain structural features at the catalytic core of the TbetaR-I are similar to tyrosine kinases rather than Ser/Thr kinases.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1999
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