Truncated trkB.T1 is a splice variant of the neurotrophin receptor trkB. In spite of its abundance, and ability to bind and internalize BDNF, it is not clear whether it can transmit BDNF signaling. We tested this hypothesis by searching for proteins binding the evolutionarily conserved cyto-domain of trkB.T1, and by studying BDNF-induced changes of gene expression through DNA microarrays. Cells bearing trkB.T1 receptors presented morphological changes. However, no cytoplasmic interactors of trkB.T1 were found. In addition, BDNF-dependent modulation of gene expression was detected in cells bearing trkB.TK but not trkB.T1 receptors. These results suggest that the main function of trkB.T1 is to regulate local availability of neurotrophins and that it is unable to sense changes in BDNF availability.

BDNF binding to truncated trkB.T1 does not affect gene expression / N. Offenhäuser, V. Muzio, S. Biffo. - In: NEUROREPORT. - ISSN 0959-4965. - 13:9(2002 Jul 02), pp. 1189-1193.

BDNF binding to truncated trkB.T1 does not affect gene expression

S. Biffo
Ultimo
2002

Abstract

Truncated trkB.T1 is a splice variant of the neurotrophin receptor trkB. In spite of its abundance, and ability to bind and internalize BDNF, it is not clear whether it can transmit BDNF signaling. We tested this hypothesis by searching for proteins binding the evolutionarily conserved cyto-domain of trkB.T1, and by studying BDNF-induced changes of gene expression through DNA microarrays. Cells bearing trkB.T1 receptors presented morphological changes. However, no cytoplasmic interactors of trkB.T1 were found. In addition, BDNF-dependent modulation of gene expression was detected in cells bearing trkB.TK but not trkB.T1 receptors. These results suggest that the main function of trkB.T1 is to regulate local availability of neurotrophins and that it is unable to sense changes in BDNF availability.
3T3 Cells; Alternative Splicing; Animals; Brain-Derived Neurotrophic Factor; Cell Size; Endocytosis; Gene Expression; Genes; Mice; Nervous System; Nervous System Diseases; Neuronal Plasticity; Neurons; Neuroprotective Agents; Protein Binding; Protein Isoforms; Protein Structure, Tertiary; RNA, Messenger; Receptor, trkB; Receptors, Cell Surface; Signal Transduction; Transcription, Genetic; Transduction, Genetic
Settore BIO/06 - Anatomia Comparata e Citologia
2-lug-2002
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/492845
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