potassium inwardly rectifying channel subfamily J member 11
آخر تحديث 16 يناير 2026
يتوافق مع الإرشادات التحريرية
- تنزيلتنزيل
- مشاركة
- Language
- نقاش
- نسخة صوتية
- أضف إلى المصادر المفضلة على جوجل
The KCNJ11 gene provides instructions for making one part (subunit) of the ATP-sensitive potassium (KATP) channels that are found in specialized pancreas cells called beta cells. These KATP channels consist of eight subunits: four of these subunits are produced from the KCNJ11 gene and four are produced from another gene called ABCC8.
Normal function
The KCNJ11 gene provides instructions for making one part (subunit) of the ATP-sensitive potassium (KATP) channels that are found in specialized pancreas cells called beta cells. These KATP channels consist of eight subunits: four of these subunits are produced from the KCNJ11 gene and four are produced from another gene called ABCC8.
These KATP channels span the cell membranes of the beta cells. Beta cells secrete the hormone insulin, which helps control the levels of glucose in the blood, also called blood sugar. Glucose is a simple sugar and the primary energy source for most cells in the body. When blood glucose levels are high, the KATP channels close, which triggers the beta cells to release insulin into the bloodstream. In this way, KATP channels help regulate insulin secretion and control blood glucose levels.
Conditions referring to this gene or chromosome
Other names
ATP-sensitive inward rectifier potassium channel 11
beta-cell inward rectifier
beta-cell inward rectifier subunit
BIR
inward rectifier K(+) channel Kir6.2
inwardly rectifying potassium channel KIR6.2
Kir6.2
potassium channel, inwardly rectifying subfamily J, member 11
potassium channel, inwardly rectifying, BIR subunit
Related patient information and medicines
Patient information leaflet
هل يمكنني تناول بيسوبرولول وراميبريل معًا؟
This might make you feel dizzy, lightheaded, or faint. It can also occasionally lead to increased levels of potassium in your blood أو affect how your kidneys work. Why this happens Both medicines work to lower blood pressure but in different ways. Bisoprolol is a beta-blocker that slows the heart rate, while ramipril is an ACE inhibitor that.
Patient information leaflet
هل يمكنني تناول أتينولول وراميبريل معًا؟
Why this happens Both medicines work to lower blood pressure but in different ways: أتينولول is a beta-blocker that slows the heart rate, while ramipril is an ACE inhibitor that relaxes blood vessels. Salt substitutes (Potassium-rich) Ramipril can increase the levels of potassium in your blood. Many salt substitutes (such as Lo-Salt) contain.
Patient information leaflet
هل يمكنني تناول بيسوبرولول ولوسارتان معًا؟
Taking bisoprolol and losartan together can cause your blood pressure to drop lower than intended. This may make you feel dizzy, lightheaded, or faint, especially when standing up quickly. 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. Bisoprolol.
Patient information leaflet
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 أو affect your kidney function, especially if you are already unwell with an infection. Salt substitutes.
Patient information leaflet
هل يمكنني تناول أملوديبين ولوسارتان معًا؟
Taking amlodipine and losartan together يمكن أن cause your ضغط الدم إلى drop lower than if you took either medicine alone. While this is often the intended goal of your treatment, it can sometimes lead to side effects like dizziness, lightheadedness, or fainting, ... High potassium levels (hyperkalaemia) Losartan can increase potassium levels in.
Patient information leaflet
هل يمكنني تناول نوستيندي وراميبريل معًا؟
Taking Nustendi and ramipril together can increase the risk of your kidneys ليست 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. إخلاء المسؤولية هذا information هو لـ general educational purposes only and should.
قراءة إضافية ومراجع
- potassium inwardly rectifying channel subfamily J member 11; MedlinePlus, National Library of Medicine.
- Bennett K, James C, Hussain K. Pancreatic beta-cell KATP channels: Hypoglycaemia and hyperglycaemia. Rev Endocr Metab Disord. 2010 Sep;11(3):157-63. doi: 10.1007/s11154-010-9144-2.
- De Leon DD, Pinney SE. Permanent Neonatal Diabetes Mellitus. 2008 Feb 8 [updated 2025 Sep 25]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1447/
- Flanagan SE, Clauin S, Bellanne-Chantelot C, de Lonlay P, Harries LW, Gloyn AL, Ellard S. Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2009 Feb;30(2):170-80. doi: 10.1002/humu.20838.
- Flanagan SE, Edghill EL, Gloyn AL, Ellard S, Hattersley AT. Mutations in KCNJ11, which encodes Kir6.2, are a common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype. Diabetologia. 2006 Jun;49(6):1190-7. doi: 10.1007/s00125-006-0246-z. Epub 2006 Apr 12.
- Gloyn AL, Siddiqui J, Ellard S. Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2006 Mar;27(3):220-31. doi: 10.1002/humu.20292.
- Golshan-Tafti M, Bahrami R, Dastgheib SA, Karimi-Zarchi M, Azizi S, Marzbanrad Z, Hajizadeh N, Aghasipour M, Yeganegi M, Shiri A, Aghili K, Neamatzadeh H. Comprehensive data on the relationship between KCNJ11 polymorphisms and gestational diabetes mellitus predisposition: a meta-analysis. J Diabetes Metab Disord. 2024 Apr 18;23(1):475-486. doi: 10.1007/s40200-024-01428-0. eCollection 2024 Jun.
- James C, Kapoor RR, Ismail D, Hussain K. The genetic basis of congenital hyperinsulinism. J Med Genet. 2009 May;46(5):289-99. doi: 10.1136/jmg.2008.064337. Epub 2009 Mar 1.
- Polak M, Cave H. Neonatal diabetes mellitus: a disease linked to multiple mechanisms. Orphanet J Rare Dis. 2007 Mar 9;2:12. doi: 10.1186/1750-1172-2-12.
- Reyes S, Park S, Johnson BD, Terzic A, Olson TM. KATP channel Kir6.2 E23K variant overrepresented in human heart failure is associated with impaired exercise stress response. Hum Genet. 2009 Dec;126(6):779-89. doi: 10.1007/s00439-009-0731-9.
- Rubio-Cabezas O, Klupa T, Malecki MT; CEED3 Consortium. Permanent neonatal diabetes mellitus--the importance of diabetes differential diagnosis in neonates and infants. Eur J Clin Invest. 2011 Mar;41(3):323-33. doi: 10.1111/j.1365-2362.2010.02409.x. Epub 2010 Nov 4.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
16 يناير 2026 | أحدث إصدار
1 Jan 2026 | نُشر في الأصل
انضم إلى المحادثة
شارك أفكارك أو تجاربك مع الآخرين في مجتمعات المرضى.
اسأل، شارك، تواصل.
تصفح المناقشات، اطرح الأسئلة، وشارك التجارب عبر مئات المواضيع الصحية.
اشترك في النشرة الإخبارية للمرضى
جرعتك الأسبوعية من النصائح الصحية الواضحة والموثوقة - مكتوبة لمساعدتك على الشعور بالاطلاع والثقة والتحكم.
من خلال الاشتراك، فإنك تقبل سياسة الخصوصية. يمكنك إلغاء الاشتراك في أي وقت. نحن لا نبيع بياناتك أبدًا.