netrin 1
Last updated 19 May 2025
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The NTN1 gene provides instructions for making a protein called netrin-1, which is involved in the development of the nervous system. This protein attaches (binds) to a protein called netrin-1 receptor, and these two proteins fit together like a lock and key. The binding of netrin-1 to its receptor helps direct the growth of specialized nerve cell extensions called axons. Axons transmit nerve impulses that can signal muscle movement.
Normal function
The NTN1 gene provides instructions for making a protein called netrin-1, which is involved in the development of the nervous system. This protein attaches (binds) to a protein called netrin-1 receptor, and these two proteins fit together like a lock and key. The binding of netrin-1 to its receptor helps direct the growth of specialized nerve cell extensions called axons. Axons transmit nerve impulses that can signal muscle movement.
When the brain sends a signal to trigger muscle movement, the signal usually travels from one half of the brain to the opposite side of the body. Binding netrin-1 to its receptor allows axons to develop this signaling pathway.
Conditions referring to this gene or chromosome
Other names
MRMV4
NET1
NTN1L
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Further reading and references
- netrin 1; MedlinePlus, National Library of Medicine.
- Boyer NP, Gupton SL. Revisiting Netrin-1: One Who Guides (Axons). Front Cell Neurosci. 2018 Jul 31;12:221. doi: 10.3389/fncel.2018.00221. eCollection 2018.
- Dun XP, Parkinson DB. Role of Netrin-1 Signaling in Nerve Regeneration. Int J Mol Sci. 2017 Feb 24;18(3):491. doi: 10.3390/ijms18030491.
- Meneret A, Franz EA, Trouillard O, Oliver TC, Zagar Y, Robertson SP, Welniarz Q, Gardner RJM, Gallea C, Srour M, Depienne C, Jasoni CL, Dubacq C, Riant F, Lamy JC, Morel MP, Guerois R, Andreani J, Fouquet C, Doulazmi M, Vidailhet M, Rouleau GA, Brice A, Chedotal A, Dusart I, Roze E, Markie D. Mutations in the netrin-1 gene cause congenital mirror movements. J Clin Invest. 2017 Nov 1;127(11):3923-3936. doi: 10.1172/JCI95442. Epub 2017 Sep 25.
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