Contactin: Difference between revisions
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== Function == | == Function == | ||
'''Contactin''' (CNTN) is a neuronal cell surface glycoprotein which associates with sodium channel and enhances the density of these channels on the plasma membrane in mammalian expression systems<ref>PMID:16029194</ref>. | '''Contactin''' (CNTN) is a neuronal cell surface glycoprotein which associates with sodium channel and enhances the density of these channels on the plasma membrane in mammalian expression systems<ref>PMID:16029194</ref>. | ||
'''Contactin-2''' is a synaptic membrane protein<ref>PMID: | *'''Contactin-2''' is a synaptic membrane protein involved in pathology of Alzheimer Disease<ref>PMID:29859129</ref>. | ||
== Disease == | == Disease == |
Revision as of 10:13, 9 June 2024
FunctionContactin (CNTN) is a neuronal cell surface glycoprotein which associates with sodium channel and enhances the density of these channels on the plasma membrane in mammalian expression systems[1].
Diseasecontactin-4 is an autism susceptibility locus[3].
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3D structures of contactin3D structures of contactin
Updated on 09-June-2024
ReferencesReferences
- ↑ Rush AM, Craner MJ, Kageyama T, Dib-Hajj SD, Waxman SG, Ranscht B. Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons. Eur J Neurosci. 2005 Jul;22(1):39-49. PMID:16029194 doi:http://dx.doi.org/10.1111/j.1460-9568.2005.04186.x
- ↑ Chatterjee M, Del Campo M, Morrema THJ, de Waal M, van der Flier WM, Hoozemans JJM, Teunissen CE. Contactin-2, a synaptic and axonal protein, is reduced in cerebrospinal fluid and brain tissue in Alzheimer's disease. Alzheimers Res Ther. 2018 Jun 1;10(1):52. PMID:29859129 doi:10.1186/s13195-018-0383-x
- ↑ Cottrell CE, Bir N, Varga E, Alvarez CE, Bouyain S, Zernzach R, Thrush DL, Evans J, Trimarchi M, Butter EM, Cunningham D, Gastier-Foster JM, McBride KL, Herman GE. Contactin 4 as an autism susceptibility locus. Autism Res. 2011 Jun;4(3):189-99. doi: 10.1002/aur.184. Epub 2011 Feb 9. PMID:21308999 doi:http://dx.doi.org/10.1002/aur.184