potassium voltage-gated channel subfamily Q member 2
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ال KCNQ2 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged atoms (ions) of potassium into and out of cells, play a key role in a cell's ability to generate and transmit electrical signals.
Normal function
ال KCNQ2 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged atoms (ions) of potassium into and out of cells, play a key role in a cell's ability to generate and transmit electrical signals.
The specific function of a potassium channel depends on its protein components and its location in the body. Channels made with the KCNQ2 protein are active in nerve cells (neurons) in the brain, where they transport potassium ions out of cells. These channels transmit a particular type of electrical signal called the M-current, which prevents the neuron from continuing to send signals to other neurons. The M-current ensures that the neuron is not constantly active, or excitable.
Potassium channels are made up of several protein components (subunits). Each channel contains four alpha subunits that form the hole (pore) through which potassium ions move. Four alpha subunits from the KCNQ2 gene can form a channel. However, the KCNQ2 alpha subunits can also interact with alpha subunits produced from the KCNQ3 gene to form a functional potassium channel, and these channels transmit a much stronger M-current.
Conditions referring to this gene or chromosome
Other names
BFNC
BFNS1
EBN
EBN1
EIEE7
ENB1
HNSPC
KCNA11
KCNQ2_HUMAN
KQT-like 2
KV7.2
KVEBN1
potassium channel, voltage gated KQT-like subfamily Q, member 2
potassium voltage-gated channel subfamily KQT member 2
potassium voltage-gated channel, KQT-like subfamily, member 2
voltage-gated potassium channel subunit Kv7.2
Related patient information and medicines
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إصابة الكلى الحادة
إصابة الكلى الحادة can be a confusing name as it suggests an accident or injury to that part of your body, eg from a fall or trauma. However, acute kidney injury is actually a condition where your kidneys suddenly stop working properly. If you have acute kidney injury (AKI) your kidneys suddenly stop working as well as they should. This means the.
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هل يمكنني تناول كو-أموكسكلاف وراميبريل معًا؟
Taking co-amoxiclav and ramipril together can occasionally increase the risk of a rare but serious allergic reaction called angioedema (swelling under the skin). It may also increase the risk of high potassium levels in the blood or affect your kidney function, especially if you are already unwell with an infection. Our Medicines Interaction.
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هل يمكنني تناول المغنيسيوم والفليكاينيد معًا؟
In some cases, magnesium can actually be helpful for heart rhythm issues, but it must be balanced correctly. Why this happens Both magnesium and flecainide affect the electrical signals and mineral channels (like sodium and potassium) in your heart cells. While they don't usually stop each other from being absorbed, having too much or too little.
Patient information leaflet
هل يمكنني تناول نوستيندي وراميبريل معًا؟
Taking Nustendi and ramipril together يمكن أن increase the risk of your kidneys not working as well as they should. It may also lead to high levels of potassium in your blood (hyperkalaemia). Why this happens Nustendi contains two medicines: bempedoic acid and ezetimibe. Bempedoic acid can sometimes increase levels of uric acid and affect kidney.
Patient information leaflet
هل يمكنني تناول بيسوبرولول ولوسارتان معًا؟
It can also lead to increased levels of potassium in your blood. Why this happens Both medicines work to lower blood pressure but in different ways. بيسوبرولول is a beta-blocker that slows the heart rate, while losartan is an angiotensin II receptor blocker (ARB) that relaxes blood vessels. When used together, their effects add up (additive.
قراءة إضافية ومراجع
- potassium voltage-gated channel subfamily Q member 2; MedlinePlus, National Library of Medicine.
- Biervert C, Schroeder BC, Kubisch C, Berkovic SF, Propping P, Jentsch TJ, Steinlein OK. A potassium channel mutation in neonatal human epilepsy. Science. 1998 Jan 16;279(5349):403-6. doi: 10.1126/science.279.5349.403.
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- Chung HJ, Jan YN, Jan LY. Polarized axonal surface expression of neuronal KCNQ channels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminal domains. Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8870-5. doi: 10.1073/pnas.0603376103. Epub 2006 May 30.
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- Saitsu H, Kato M, Koide A, Goto T, Fujita T, Nishiyama K, Tsurusaki Y, Doi H, Miyake N, Hayasaka K, Matsumoto N. Whole exome sequencing identifies KCNQ2 mutations in Ohtahara syndrome. Ann Neurol. 2012 Aug;72(2):298-300. doi: 10.1002/ana.23620. No abstract available.
- Schroeder BC, Kubisch C, Stein V, Jentsch TJ. Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. Nature. 1998 Dec 17;396(6712):687-90. doi: 10.1038/25367.
- Singh NA, Westenskow P, Charlier C, Pappas C, Leslie J, Dillon J, Anderson VE, Sanguinetti MC, Leppert MF; BFNC Physician Consortium. KCNQ2 and KCNQ3 potassium channel genes in benign familial neonatal convulsions: expansion of the functional and mutation spectrum. Brain. 2003 Dec;126(Pt 12):2726-37. doi: 10.1093/brain/awg286. Epub 2003 Oct 8.
- Soldovieri MV, Miceli F, Bellini G, Coppola G, Pascotto A, Taglialatela M. Correlating the clinical and genetic features of benign familial neonatal seizures (BFNS) with the functional consequences of underlying mutations. Channels (Austin). 2007 Jul-Aug;1(4):228-33. doi: 10.4161/chan.4823. Epub 2007 Aug 2.
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- Wang HS, Pan Z, Shi W, Brown BS, Wymore RS, Cohen IS, Dixon JE, McKinnon D. KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel. Science. 1998 Dec 4;282(5395):1890-3. doi: 10.1126/science.282.5395.1890.
- Weckhuysen S, Mandelstam S, Suls A, Audenaert D, Deconinck T, Claes LR, Deprez L, Smets K, Hristova D, Yordanova I, Jordanova A, Ceulemans B, Jansen A, Hasaerts D, Roelens F, Lagae L, Yendle S, Stanley T, Heron SE, Mulley JC, Berkovic SF, Scheffer IE, de Jonghe P. KCNQ2 encephalopathy: emerging phenotype of a neonatal epileptic encephalopathy. Ann Neurol. 2012 Jan;71(1):15-25. doi: 10.1002/ana.22644.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
18 Aug 2020 | أحدث إصدار
1 Apr 2013 | نُشر في الأصل
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