The Trk family of neurotrophin receptors

Wiley - Tập 25 Số 11 - Trang 1386-1403 - 1994
Mariano Barbacid1
1Department of Molecular Biology, Bristol-Myers-Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000.

Tóm tắt

AbstractAccumulating evidence indicates that the Trk family of tyrosine protein kinase receptors, Trk (also known as TrkA), TrkB, and TrkC, are responsible for mediating the trophic effects of the NGF family of neurotrophins. Nerve growth factor (NGF) specifically recognizes Trk, a receptor indentified in all major NGF targets, including sympathetic, trigeminal, and dorsal root ganglia as well as in cholinergic neurons of the basal forebrain and the striatum. Brain‐derived neurotropic factor (BDNF) and neurotrophin‐4 (NT‐4) specifically activate the TrkB tyrosine kinase receptor. trkB transcripts encoding this receptor are found throughout multiple structure of the central and peripheral nervous system. Neurotrophin‐3 (NT‐3) primarily activates the TrkC tyrosine protein kinases, four related isoforns encoded by alternative splicing of trkC, a gene also wildely expressed throughtout the mammalian nervous system. Unlike the other neurotrophins, NT‐3 appears to be somewhat promiscuous since it can activate Trk and TrkB kinase receptors, at least in certain cell systems. The trkB and trkC genes also encode noncatalytic neurotrophin receptor isoforms of an as yet, unknown function. Recently, strains of mice lacking each of these tyrosine kinase receptors have been generated. Preliminary characterization of these mutant mice has provided significant information regarding the role of these receptors in the ontogeny of the mammlian nervous system. For instance, mice deficient for Trk receptors lack most sympathetic neurons and do not display nociceptive and temperature sensations, two defects likely to result from severe neuronal cell loss in their trigeminal and dorsal root ganglia. Mice lacking TrkB tyrosine kinase receptors die postnatally due to their inability to intake food. Neuron cell loss in their trigeminal, nodose and pretrosal sensory ganglia as well as in the facial motor nucleus are likely to contribute to this phenotype. Finally, TrkC‐deficient mice display strikingly abnormal movements consistent with loss of proprioception, a defect likely to be a consequence of the complete loss of Ia muscle afferents observed in this mutant mice. 1994 John Wiley & Sons, Inc.

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Tài liệu tham khảo

Barbacid M., 1993, Nerve growth factor: a tale of two receptors, Oncogene, 8, 2033

Barbacid M., 1993, Molicular Genetics of Nervous System Tumors, 123

10.1016/S0021-9258(18)82449-8

Bech K. D., 1993, Induction of noncatalytic TrkB neurotrophin receptors during axonal sprouting in the adult hippocampus, J. Neurosci., 13, 4001, 10.1523/JNEUROSCI.13-09-04001.1993

10.1016/0896-6273(91)90287-A

10.1242/dev.119.3.597

10.1016/0896-6273(92)90040-K

10.1016/0092-8674(91)90149-S

Coulier F., 1990, Human trk oncogenes activated by point mutation, in ‐frame deletion, and duplication of the tyrosine kinase domain. Mol., Cell. Biol., 140, 4202

10.1097/00001756-199308000-00007

10.1038/365781a0

10.1073/pnas.90.23.10984

10.1073/pnas.90.12.5423

Frisen J., 1993, Characterization of glial trk B receptors: differential response to injury in the central and peripheral nervous system, Proc. Natl. Acad. Sci. USA, 90, 4971, 10.1073/pnas.90.11.4971

10.1083/jcb.123.2.455

10.1016/0092-8674(91)90629-D

10.1002/ana.410270313

Hardie D. G., 1994, Protein Kinase Factsbook

10.1038/350678a0

10.1016/0896-6273(92)90184-F

Horigome K., 1993, Mediator release form mast cells by nerve growth factor. neurotrophin specificity and receptor mediation, J. Biol. Chem., 268, 14881, 10.1016/S0021-9258(18)82415-2

10.1073/pnas.89.7.3060

10.1016/0896-6273(93)90306-C

10.1002/neu.480240907

10.1016/0896-6273(92)90066-M

10.1038/350158a0

10.1126/science.1850549

Klein R., 1989, trk B, a novel tyrosine protein kinase receptor expressed during mouse neural development, EMBO J., 8, 3701, 10.1002/j.1460-2075.1989.tb08545.x

10.1016/0092-8674(90)90476-U

Klein R., 1990, Expression of the tyrosine kinase receptor gene trk B is confined to the murine embryonic and adult nervous system, Development, 109, 845, 10.1242/dev.109.4.845

10.1016/0092-8674(91)90419-Y

10.1016/0092-8674(91)90628-C

10.1016/0896-6273(92)90209-V

Klein R., 1993, Targeted disruption of the trk B neurotropin receptor gene results in nervous system lesions and neonatal death, Cell, 75, 113, 10.1016/S0092-8674(05)80088-1

10.1038/368249a0

10.1016/0092-8674(91)90442-2

10.1002/j.1460-2075.1993.tb05977.x

10.1523/JNEUROSCI.14-01-00014.1994

10.1016/0092-8674(92)90286-L

10.1126/science.8128229

10.1126/science.3306916

10.1126/science.1604323

Lindsay R. M., 1994, Neurotrophic factors: from molecule to man, Trends Genetics, 17, 182

10.1016/0092-8674(91)90441-Z

10.1016/0896-6273(92)90065-L

10.1038/319743a0

Martin‐Zanca D., 1989, Molicular and biochemical characterization of the human trk protooncogene. Mol., Cell. Biol., 9, 24

10.1101/gad.4.5.683

10.1016/0166-2236(92)90047-C

10.1073/pnas.89.6.2374

10.1016/0306-4522(92)90292-A

10.1016/0896-6273(93)90307-D

Middlemas D. S., 1991, trk B, a neural receptor protein‐tyrosine kinase: evidence for a full‐length and two truncated receptors. Mol., Cell. Biol., 11, 143

10.1523/JNEUROSCI.13-09-04029.1993

Muroya K., 1992, Nerve growth factor induces rapid accumulation of the GTP‐bound form of p21ras in rat pheochromocytoma PC12 cells, Oncogene, 7, 277

10.1016/S0021-9258(19)49410-6

10.1016/0006-291X(91)91357-I

10.1016/0896-6273(92)90039-G

10.1021/bi00131a019

10.1016/0092-8674(92)90536-L

10.1016/0896-6273(91)90339-2

Rabin S. J., 1993, SNT, a differentiation‐specific target of neurotrophic factor‐induced tyrosine kinase activity in neurons and PC12 cells. Mol., Cell. Biol., 13, 2203

10.1016/0896-6273(91)90232-O

10.1016/0896-6273(92)90177-F

Schneider R., 1991, A novel modular mosaic of cell adhesion motifs in the extracellular domains of the neurogenic trk and trk B tryrosine kinase receptors, Oncogene, 6, 1807

10.1002/jnr.490360402

10.1038/368246a0

10.1016/S0733-8619(18)30206-8

10.1016/0092-8674(94)90048-5

Soltoff S. P., 1992, Nerve growth factor promotes the activation of phosphatidylinositol 3‐kinase and its association with the trk tyrosine kinase, J. Cell Biol., 267, 17472

10.1016/0092-8674(91)90396-G

10.1016/0092-8674(91)90395-F

10.1016/0006-8993(93)91681-H

10.1016/0896-6273(94)90223-2

Suen K. L., 1993, Molicular cloning of the mouse grb 2 gene: differential interaction of the Grb2 adaptor protein with eqidermal interaction of the Grb2 adaptor protein with epidermal growth factor and nerve growth factor receptors. Mol., Cell. Biol., 13, 5500

Tapley P., 1992, K252a is a selective inhibitor of the tyrosine protein kinase activity of the trk family of oncogenes and neurotrophin receptors, Oncogene, 7, 371

Tessarollo L., 1993, trk C, a receptor for neurotrophin‐3, is widely expressed in the developing nervous system and in non‐neuronal tissues, Development, 118, 463, 10.1242/dev.118.2.463

10.1016/0092-8674(92)90075-N

10.1016/0896-6273(93)90212-A

10.1016/0896-6273(93)90211-9

10.1097/00001756-199110000-00010

10.1097/00001756-199307000-00031

10.1073/pnas.88.13.5650

10.1111/j.1471-4159.1993.tb03496.x

10.1016/0378-5955(93)90202-C

10.1006/dbio.1993.1224

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Wiley

Tập 25 Số 11

1386-1403

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