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Artemin activates axonal growth via SFK and ERK‐dependent signalling pathways in mature dorsal root ganglia neurons
Author(s) -
Jeong Doc Gyun,
Park Wyun Kon,
Park Seyeon
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1436
Subject(s) - microbiology and biotechnology , proto oncogene tyrosine protein kinase src , sh3 domain , src family kinase , signal transducing adaptor protein , glial cell line derived neurotrophic factor , gdnf family of ligands , biology , actin cytoskeleton , kinase , mapk/erk pathway , signal transduction , chemistry , neurotrophic factors , cytoskeleton , receptor , biochemistry , cell
Artemin, one of the glial cell line‐derived neurotrophic factor (GDNF) family, enhances the generation and survival of early sympathetic neurons and superior cervical ganglion (SCG) neurons. Src‐family kinases (SFK) are involved in the growth and differentiation of cells, which are composed of unique Src homology 2 (SH2), Src homology 3 (SH3) and kinase domains. Various extra‐cellular molecules containing growth factors and G‐protein coupled receptors stimulate SFK. In this report, artemin is shown to have a significant effect on the neurite growth of dorsal root ganglia (DRG) neurons. Also, artemin triggers Src‐family kinase activation and the phosphorylation of extra‐cellular signal‐regulated kinases (ERK) mitogen‐activated protein kinase (MAPK). Artemin also regulated actin polymerization. There are several indications that another SH3‐containing protein, Hck, and an SH3‐containing adaptor protein, Nck1, play an important role in the organization of the actin cytoskeleton by cellular signalling. These findings suggest that the exploration of binding partners for the SH3 domain could provide an insight into regulation between the microtubule and actin networks. The binding partners for the SH3 domains of Nck, Src and Hck that we identified were Smc chromosome segregation ATPases, FOG Zn‐finger protein and the FYVE zinc‐binding domain, respectively. Copyright © 2007 John Wiley & Sons, Ltd.