GFR alpha3, a component of the artemin receptor, is required for migration and survival of the superior cervical ganglion - PubMed (original) (raw)
GFR alpha3, a component of the artemin receptor, is required for migration and survival of the superior cervical ganglion
J Nishino et al. Neuron. 1999 Aug.
Free article
Abstract
GFR alpha3 is a component of the receptor for the neurotrophic factor artemin. The role of GFR alpha3 in nervous system development was examined by generating mice in which the Gfr alpha3 gene was disrupted. The Gfr alpha3-/- mice exhibited severe defects in the superior cervical ganglion (SCG), whereas other ganglia appeared normal. SCG precursor cells in the mutant embryos failed to migrate to the correct position, and they subsequently failed to innervate the target organs. In wild-type embryos, Gfr alpha3 was expressed in migrating SCG precursors, and artemin was expressed in and near the SCG. After birth, SCG neurons in the mutant mice underwent progressive cell death. These observations suggest that GFR alpha3-mediated signaling is required both for the rostral migration of SCG precursors and for the survival of mature SCG neurons.
Similar articles
- NGF utilizes c-Ret via a novel GFL-independent, inter-RTK signaling mechanism to maintain the trophic status of mature sympathetic neurons.
Tsui-Pierchala BA, Milbrandt J, Johnson EM Jr. Tsui-Pierchala BA, et al. Neuron. 2002 Jan 17;33(2):261-73. doi: 10.1016/s0896-6273(01)00585-2. Neuron. 2002. PMID: 11804573 - Sympathetic neuron survival and TrkA expression in NT3-deficient mouse embryos.
Wyatt S, Piñon LG, Ernfors P, Davies AM. Wyatt S, et al. EMBO J. 1997 Jun 2;16(11):3115-23. doi: 10.1093/emboj/16.11.3115. EMBO J. 1997. PMID: 9214629 Free PMC article. - Neurturin shares receptors and signal transduction pathways with glial cell line-derived neurotrophic factor in sympathetic neurons.
Creedon DJ, Tansey MG, Baloh RH, Osborne PA, Lampe PA, Fahrner TJ, Heuckeroth RO, Milbrandt J, Johnson EM Jr. Creedon DJ, et al. Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):7018-23. doi: 10.1073/pnas.94.13.7018. Proc Natl Acad Sci U S A. 1997. PMID: 9192684 Free PMC article. - Other neurotrophic factors: glial cell line-derived neurotrophic factor (GDNF).
Saarma M, Sariola H. Saarma M, et al. Microsc Res Tech. 1999 May 15-Jun 1;45(4-5):292-302. doi: 10.1002/(SICI)1097-0029(19990515/01)45:4/5<292::AID-JEMT13>3.0.CO;2-8. Microsc Res Tech. 1999. PMID: 10383122 Review. - The GDNF receptor: recent progress and unanswered questions.
Mason I. Mason I. Mol Cell Neurosci. 1996;8(2-3):112-9. doi: 10.1006/mcne.1996.0050. Mol Cell Neurosci. 1996. PMID: 8918828 Review. No abstract available.
Cited by
- Neuro-mesenchymal units control ILC2 and obesity via a brain-adipose circuit.
Cardoso F, Klein Wolterink RGJ, Godinho-Silva C, Domingues RG, Ribeiro H, da Silva JA, Mahú I, Domingos AI, Veiga-Fernandes H. Cardoso F, et al. Nature. 2021 Sep;597(7876):410-414. doi: 10.1038/s41586-021-03830-7. Epub 2021 Aug 18. Nature. 2021. PMID: 34408322 Free PMC article. - Hallmarks of cancer-the new testament.
Senga SS, Grose RP. Senga SS, et al. Open Biol. 2021 Jan;11(1):200358. doi: 10.1098/rsob.200358. Epub 2021 Jan 20. Open Biol. 2021. PMID: 33465324 Free PMC article. Review. - Roles of the RET Proto-oncogene in Cancer and Development.
Takahashi M, Kawai K, Asai N. Takahashi M, et al. JMA J. 2020 Jul 15;3(3):175-181. doi: 10.31662/jmaj.2020-0021. Epub 2020 Jul 7. JMA J. 2020. PMID: 33150251 Free PMC article. Review. - Development of the Autonomic Nervous System: Clinical Implications.
Lefcort F. Lefcort F. Semin Neurol. 2020 Oct;40(5):473-484. doi: 10.1055/s-0040-1713926. Epub 2020 Sep 14. Semin Neurol. 2020. PMID: 32927484 Free PMC article. Review. - The role of glial cell line-derived neurotrophic factor family member artemin in neurological disorders and cancers.
Zhu S, Li Y, Bennett S, Chen J, Weng IZ, Huang L, Xu H, Xu J. Zhu S, et al. Cell Prolif. 2020 Jul;53(7):e12860. doi: 10.1111/cpr.12860. Epub 2020 Jun 23. Cell Prolif. 2020. PMID: 32573073 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases