sodium voltage-gated channel alpha subunit 10
آخر تحديث 18 Aug 2020
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ال SCN10A gene belongs to a family of genes that provide instructions for making sodium channels. These channels, which transport positively charged sodium atoms (sodium ions) into cells, play a key role in a cell's ability to generate and transmit electrical signals.
Normal function
ال SCN10A gene belongs to a family of genes that provide instructions for making sodium channels. These channels, which transport positively charged sodium atoms (sodium ions) into cells, play a key role in a cell's ability to generate and transmit electrical signals.
ال SCN10A gene provides instructions for making one part (the alpha subunit) of a sodium channel called NaV1.8. NaV1.8 sodium channels are found in nerve cells called nociceptors that transmit pain signals. Nociceptors are part of the peripheral nervous system, which connects the brain and spinal cord to cells that detect sensations such as touch, smell, and pain. Nociceptors are primarily involved in transmitting pain signals. The centers of nociceptors, known as the cell bodies, are located in a part of the spinal cord called the dorsal root ganglion. Fibers called axons extend from the cell bodies, reaching throughout the body to receive sensory information. In addition to nociceptors, NaV1.8 sodium channels have also been found in heart muscle cells where, by controlling the flow of sodium ions, they likely play a role in maintaining a normal heart rhythm.
Conditions referring to this gene or chromosome
Other names
hPN3
Nav1.8
peripheral nerve sodium channel 3
PN3
SCNAA_HUMAN
sodium channel protein type 10 subunit alpha
sodium channel protein type X subunit alpha
sodium channel, voltage gated, type X alpha subunit
sodium channel, voltage-gated, type X, alpha polypeptide
sodium channel, voltage-gated, type X, alpha subunit
voltage-gated sodium channel subunit alpha Nav1.8
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قراءة إضافية ومراجع
- sodium voltage-gated channel alpha subunit 10; MedlinePlus, National Library of Medicine.
- Chambers JC, Zhao J, Terracciano CM, Bezzina CR, Zhang W, Kaba R, Navaratnarajah M, Lotlikar A, Sehmi JS, Kooner MK, Deng G, Siedlecka U, Parasramka S, El-Hamamsy I, Wass MN, Dekker LR, de Jong JS, Sternberg MJ, McKenna W, Severs NJ, de Silva R, Wilde AA, Anand P, Yacoub M, Scott J, Elliott P, Wood JN, Kooner JS. Genetic variation in SCN10A influences cardiac conduction. Nat Genet. 2010 Feb;42(2):149-52. doi: 10.1038/ng.516. Epub 2010 Jan 10.
- Faber CG, Lauria G, Merkies IS, Cheng X, Han C, Ahn HS, Persson AK, Hoeijmakers JG, Gerrits MM, Pierro T, Lombardi R, Kapetis D, Dib-Hajj SD, Waxman SG. Gain-of-function Nav1.8 mutations in painful neuropathy. Proc Natl Acad Sci U S A. 2012 Nov 20;109(47):19444-9. doi: 10.1073/pnas.1216080109. Epub 2012 Oct 31.
- Facer P, Punjabi PP, Abrari A, Kaba RA, Severs NJ, Chambers J, Kooner JS, Anand P. Localisation of SCN10A gene product Na(v)1.8 and novel pain-related ion channels in human heart. Int Heart J. 2011;52(3):146-52. doi: 10.1536/ihj.52.146.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
18 Aug 2020 | أحدث إصدار
1 Nov 2012 | نُشر في الأصل
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