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<scene name='57/579704/Dimer_basic_view/3'>Just trying a scene</scene> | <scene name='57/579704/Dimer_basic_view/3'>Just trying a scene</scene> | ||
Revision as of 18:53, 11 May 2014
| This Sandbox is Reserved from 01/04/2014, through 30/06/2014 for use in the course "510042. Protein structure, function and folding" taught by Prof Adrian Goldman, Tommi Kajander, Taru Meri, Konstantin Kogan and Juho Kellosalo at the University of Helsinki. This reservation includes Sandbox Reserved 923 through Sandbox Reserved 947. |
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Introduction
Ciliary Neurotrophic Factor (CNTF) is a nerve growth factor belonging to the Interleukin-6 (IL-6) family of neuropoietic cytokines. Other members of this family include leukemia inhibitory factor (LIF), IL-6, IL-11 and oncostatin M [1].
CNTF exerts its biological function by binding into a tripartite receptor complex consisting of a specific CNTF receptor subunit α (CNTFRα) linked to the cell membrane with a glycosyl-phosphatidylinositol linkage, and two signal-transducing transmembrane subunits LIF receptor beta (LIFRβ) and gp130. Binding of a hCNTF dimer to CNTFRα is the absolute first requirement to initiate a signal transduction cascade, which ultimately results in the enhanced transcription of genes encoding e.g. acute phase plasma proteins, and suppressors of cytokine signaling. CNTFRα has been observed to exist also as a soluble receptor (sCNTFRα) (Panayotatos et al. 1994), attributed to a phospholipase C-mediated cleavage (Davis et al. 1993). Additionally, hCNTF has been observed to be able to bind both to membrane-bound and soluble human Interleukin-6 receptor (IL-6R) and use as a substitute it to form the receptor complex necessary for signal transduction (Schuster et al. 2003, [2]. These observations are considered to offer explanation as to why cells expressing LIFRβ and gp130 but not CNTFRα, are nonetheless responsive to CNTF.
CNTF's known biological functions involve affecting the growth, differentiation, survival and repair of various types of neurons and glial cells in both the central and peripheral nervous systems ([3] [2]; evidence also suggests CNTF to be expressed in other tissues, such as adipocytes and hepatocytes among others (). As the transcription of CNTF mRNA and CNTF distribution have been noticed to be altered upon neural injury, it has been suggested, that CNTF is not an absolute requirement for neural development, but in fact mainly acts in response to neural injuries and stresses . Furthermore, mice homozygous for an inactived CNTF gene have been observed to develop normally, and to display losses in motor neurons only later during adulthood. Although humans homozygous for an inactivated CNTF gene caused by a mutation have not been observed to suffer from major neurological abnormalities [1], this has been linked with early onset of amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) [2]. However, mice that have a CNTFRα knock-out die already during the perinatal stage and exhibit severe motor neuron deficits [3], suggesting that CNTFRα might have a second ligand.
Fig. 1 X-ray structure of a truncated form of hCNTF (2-187)
Structure
Overview
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