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A splice variant of the neurotrophin receptor trkB with increased specificity for brain‐derived neurotrophic factor.
Author(s) -
Strohmaier C.,
Carter B. D.,
Urfer R.,
Barde Y. A.,
Dechant G.
Publication year - 1996
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1996.tb00698.x
Subject(s) - planck , physics , library science , quantum mechanics , computer science
The trkB gene codes for a receptor tyrosine kinase, which is essential for the development of the peripheral nervous system. This receptor can be activated by three different neurotrophins: BDNF, NT‐4/5 and NT‐3. The extracellular domain of trkB was found to be encoded in 10 exons corresponding to receptor subdomains previously identified on the basis of protein sequence comparisons. Exon 9 was skipped in a novel tyrosine kinase transcript of the trkB gene, designated ctrkB‐Short (ctrkB‐S). While the previously described trkB receptor ctrkB‐Long (ctrkB‐L) and trkB‐S receptors were activated similarly by BDNF, trkB‐S interacted poorly with NT‐4/5 and NT‐3 as measured by ligand binding, ligand‐induced autophosphorylation and ligand‐dependent activation of p21ras. Efficient activation of ctrkB‐S by NT‐3 was restored by a single amino acid replacement in NT‐3 (D15A). Both trkB‐L and trkB‐S transcripts were detected in embryonic neurons.