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Specificity of neurotrophin‐3 determined by loss‐of‐function mutagenesis
Author(s) -
Kullander Klas,
Kylberg Annika,
Ebendal Ted
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19971101)50:3<496::aid-jnr16>3.0.co;2-4
Subject(s) - tropomyosin receptor kinase a , neurotrophin 3 , neurotrophin , tropomyosin receptor kinase c , nerve growth factor , receptor , loss function , function (biology) , biology , chemistry , neurotrophic factors , microbiology and biotechnology , biochemistry , brain derived neurotrophic factor , growth factor , gene , platelet derived growth factor receptor , phenotype
Neurotrophin‐3 (NT‐3) is a member of the family of neurotrophic factors, which also includes nerve growth factor (NGF) and which have specific activities on different subsets of vertebrate neurons. The aim of this study was to determine which residues in NT‐3 direct its specificity to the cognate TrkC receptor. It was possible to replace 80% of the residues in NT‐3 with NGF residues without loss of specific activity. Residues D72, Y85, R87, W101, S107, and A111, together with either the residues F12, V18, V20, M37, V42, F54, and K57 or the variable regions IV and V, accounted for the specificity of NT‐3. It is concluded that NGF and NT‐3 use overlapping as well as separated regions for determination of specificities for their cognate receptors TrkA and TrkC, respectively. J. Neurosci. Res. 50:496–503, 1997. © 1997 Wiley‐Liss, Inc.