The ADAMs family: coordinators of nervous system development, plasticity and repair |
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Authors: | Yang Peng Baker K Adam Hagg Theo |
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Affiliation: | Kentucky Spinal Cord Injury Research Center, Department of Neurological Surgery, University of Louisville, Louisville, KY 40292, USA. |
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Abstract: | A disintegrin and metalloprotease (ADAM) transmembrane proteins have metalloprotease, integrin-binding, intracellular signaling and cell adhesion activities. In contrast to other metalloproteases, ADAMs are particularly important for cleavage-dependent activation of proteins such as Notch, amyloid precursor protein (APP) and transforming growth factor alpha (TGFalpha), and can bind integrins. Not surprisingly, ADAMs have been shown or suggested to play important roles in the development of the nervous system, where they regulate proliferation, migration, differentiation and survival of various cells, as well as axonal growth and myelination. On the eleventh anniversary of the naming of this family of proteins, the relatively unknown ADAMs are emerging as potential therapeutic targets for neural repair. For example, over-expression of ADAM10, one of the alpha-secretases for APP, can prevent amyloid formation and hippocampal defects in an Alzheimer mouse model. Another example of this potential neural repair role is the finding that ADAM21 is uniquely associated with neurogenesis and growing axons of the adult brain. This comprehensive review will discuss the growing literature about the roles of ADAMs in the developing and adult nervous system, and their potential roles in neurological disorders. Most excitingly, the expanding understanding of their normal roles suggests that they can be manipulated to promote neural repair in the degenerating and injured adult nervous system. |
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Keywords: | ADAM, a disintegrin and metalloprotease ADAMTS, a disintegrin and metalloprotease with thrombospondin motifs APP, amyloid precursor protein C. elegans, Caenorhabditis elegans CD, cluster of differentiation CHL1, close homologue of the neural cell adhesion molecule L1 CNS, central nervous system DG, dentate gyrus E, embryonic day EAE, experimental autoimmune encephalomyelitis ECM, extracellular matrix EGF, epidermal growth factor EGFR, epidermal growth factor receptor erbB, avian erythroblastosis oncogene B HB-EGF, heparin-binding epidermal growth factor-like growth factor MMP, matrix metalloprotease mRNA, messenger ribonucleic acid NGF, nerve growth factor ND, not determined P, postnatal day PI-3K, phosphoinositide-3 kinase Robo, roundabout RMS, rostral migratory stream SVZ, subventricular zone TACE, tumor necrosis factor alpha converting enzyme TIMP, tissue inhibitor of metalloprotease SH3, src homology region 3 TGF, transforming growth factor TNF, tumor necrosis factor VCAM-1, vascular cell adhesion molecule-1 |
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