TNFRSF19
Tumor necrosis factor receptor superfamily, member 19, also known as TNFRSF19 and TROY is a human gene.[5]
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is highly expressed during embryonic development. It has been shown to interact with TNF receptor associated factor (TRAF) family members, and to activate c-Jun N-terminal kinases (JNK) signaling pathway when overexpressed in cells. This receptor is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. Alternatively spliced transcript variants encoding distinct isoforms have been described.[5]
See also
- Mitogen-activated protein kinase for JNK signaling pathway description
References
- GRCh38: Ensembl release 89: ENSG00000127863 - Ensembl, May 2017
- GRCm38: Ensembl release 89: ENSMUSG00000060548 - Ensembl, May 2017
- "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- "Entrez Gene: TNFRSF19 tumor necrosis factor receptor superfamily, member 19".
Further reading
- Robertson NG, Khetarpal U, Gutiérrez-Espeleta GA, et al. (1995). "Isolation of novel and known genes from a human fetal cochlear cDNA library using subtractive hybridization and differential screening". Genomics. 23 (1): 42–50. doi:10.1006/geno.1994.1457. PMID 7829101.
- Kojima T, Morikawa Y, Copeland NG, et al. (2000). "TROY, a newly identified member of the tumor necrosis factor receptor superfamily, exhibits a homology with Edar and is expressed in embryonic skin and hair follicles". J. Biol. Chem. 275 (27): 20742–7. doi:10.1074/jbc.M002691200. PMID 10764796.
- Eby MT, Jasmin A, Kumar A, et al. (2000). "TAJ, a novel member of the tumor necrosis factor receptor family, activates the c-Jun N-terminal kinase pathway and mediates caspase-independent cell death". J. Biol. Chem. 275 (20): 15336–42. doi:10.1074/jbc.275.20.15336. PMID 10809768.
- Naito A, Yoshida H, Nishioka E, et al. (2002). "TRAF6-deficient mice display hypohidrotic ectodermal dysplasia". Proc. Natl. Acad. Sci. U.S.A. 99 (13): 8766–71. doi:10.1073/pnas.132636999. PMC 124373. PMID 12060722.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Clark HF, Gurney AL, Abaya E, et al. (2003). "The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment". Genome Res. 13 (10): 2265–70. doi:10.1101/gr.1293003. PMC 403697. PMID 12975309.
- Zhang Z, Henzel WJ (2005). "Signal peptide prediction based on analysis of experimentally verified cleavage sites". Protein Sci. 13 (10): 2819–24. doi:10.1110/ps.04682504. PMC 2286551. PMID 15340161.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
- Park JB, Yiu G, Kaneko S, et al. (2005). "A TNF receptor family member, TROY, is a coreceptor with Nogo receptor in mediating the inhibitory activity of myelin inhibitors". Neuron. 45 (3): 345–51. doi:10.1016/j.neuron.2004.12.040. PMID 15694321.
- Shao Z, Browning JL, Lee X, et al. (2005). "TAJ/TROY, an orphan TNF receptor family member, binds Nogo-66 receptor 1 and regulates axonal regeneration". Neuron. 45 (3): 353–9. doi:10.1016/j.neuron.2004.12.050. PMID 15694322.
- Spanjaard RA, Whren KM, Graves C, Bhawan J (2007). "Tumor necrosis factor receptor superfamily member TROY is a novel melanoma biomarker and potential therapeutic target". Int. J. Cancer. 120 (6): 1304–10. doi:10.1002/ijc.22367. PMID 17187358.
- Satoh J, Tabunoki H, Yamamura T, et al. (2007). "TROY and LINGO-1 expression in astrocytes and macrophages/microglia in multiple sclerosis lesions". Neuropathol. Appl. Neurobiol. 33 (1): 99–107. doi:10.1111/j.1365-2990.2006.00787.x. PMID 17239012.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.