potassium inwardly rectifying channel subfamily J member 2
Last updated 27 Jun 2022
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The KCNJ2 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged potassium ions out of cells, play key roles in a cell's ability to generate and transmit electrical signals.
Normal function
The KCNJ2 gene belongs to a large family of genes that provide instructions for making potassium channels. These channels, which transport positively charged potassium ions out of cells, play key roles 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 KCNJ2 protein are active in muscles used for movement (skeletal muscles) and in heart (cardiac) muscle. In skeletal muscle, these channels play an important role in the pattern of muscle tensing (contraction) and relaxation that allows the body to move. In the heart, the channels are involved in recharging the cardiac muscle after each heartbeat to maintain a regular rhythm. Channels formed with the KCNJ2 protein may also be involved in bone development, but their role in this process is unclear.
Researchers have determined that a molecule called PIP2 must attach (bind) to channels made with the KCNJ2 protein for the channels to function normally. PIP2 activates the ion channel and helps it stay open, which allows ions to flow across the cell membrane.
Conditions referring to this gene or chromosome
Other names
cardiac inward rectifier potassium channel
HHBIRK1
HHIRK1
HIRK1
inward rectifier K+ channel KIR2.1
IRK1
IRK2_HUMAN
KIR2.1
LQT7
potassium channel, inwardly rectifying subfamily J, member 2
potassium inwardly-rectifying channel J2
potassium inwardly-rectifying channel, subfamily J, member 2
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Further reading and references
- potassium inwardly rectifying channel subfamily J member 2; MedlinePlus, National Library of Medicine.
- Bendahhou S, Donaldson MR, Plaster NM, Tristani-Firouzi M, Fu YH, Ptacek LJ. Defective potassium channel Kir2.1 trafficking underlies Andersen-Tawil syndrome. J Biol Chem. 2003 Dec 19;278(51):51779-85. doi: 10.1074/jbc.M310278200. Epub 2003 Oct 1.
- Casini S, Postma AV. Decreased inward rectification of Kir2.1 channels is a novel mechanism underlying the short QT syndrome. Cardiovasc Res. 2012 Mar 15;93(4):535-6. doi: 10.1093/cvr/cvs084. Epub 2012 Feb 5. No abstract available.
- Chun TU, Epstein MR, Dick M 2nd, Andelfinger G, Ballester L, Vanoye CG, George AL Jr, Benson DW. Polymorphic ventricular tachycardia and KCNJ2 mutations. Heart Rhythm. 2004 Jul;1(2):235-41. doi: 10.1016/j.hrthm.2004.02.017.
- Donaldson MR, Jensen JL, Tristani-Firouzi M, Tawil R, Bendahhou S, Suarez WA, Cobo AM, Poza JJ, Behr E, Wagstaff J, Szepetowski P, Pereira S, Mozaffar T, Escolar DM, Fu YH, Ptacek LJ. PIP2 binding residues of Kir2.1 are common targets of mutations causing Andersen syndrome. Neurology. 2003 Jun 10;60(11):1811-6. doi: 10.1212/01.wnl.0000072261.14060.47.
- Hattori T, Makiyama T, Akao M, Ehara E, Ohno S, Iguchi M, Nishio Y, Sasaki K, Itoh H, Yokode M, Kita T, Horie M, Kimura T. A novel gain-of-function KCNJ2 mutation associated with short-QT syndrome impairs inward rectification of Kir2.1 currents. Cardiovasc Res. 2012 Mar 15;93(4):666-73. doi: 10.1093/cvr/cvr329. Epub 2011 Dec 8.
- Kimura H, Zhou J, Kawamura M, Itoh H, Mizusawa Y, Ding WG, Wu J, Ohno S, Makiyama T, Miyamoto A, Naiki N, Wang Q, Xie Y, Suzuki T, Tateno S, Nakamura Y, Zang WJ, Ito M, Matsuura H, Horie M. Phenotype variability in patients carrying KCNJ2 mutations. Circ Cardiovasc Genet. 2012 Jun;5(3):344-53. doi: 10.1161/CIRCGENETICS.111.962316. Epub 2012 May 15.
- Nguyen HL, Pieper GH, Wilders R. Andersen-Tawil syndrome: clinical and molecular aspects. Int J Cardiol. 2013 Dec 5;170(1):1-16. doi: 10.1016/j.ijcard.2013.10.010.
- Plaster NM, Tawil R, Tristani-Firouzi M, Canun S, Bendahhou S, Tsunoda A, Donaldson MR, Iannaccone ST, Brunt E, Barohn R, Clark J, Deymeer F, George AL Jr, Fish FA, Hahn A, Nitu A, Ozdemir C, Serdaroglu P, Subramony SH, Wolfe G, Fu YH, Ptacek LJ. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome. Cell. 2001 May 18;105(4):511-9. doi: 10.1016/s0092-8674(01)00342-7.
- Priori SG, Pandit SV, Rivolta I, Berenfeld O, Ronchetti E, Dhamoon A, Napolitano C, Anumonwo J, di Barletta MR, Gudapakkam S, Bosi G, Stramba-Badiale M, Jalife J. A novel form of short QT syndrome (SQT3) is caused by a mutation in the KCNJ2 gene. Circ Res. 2005 Apr 15;96(7):800-7. doi: 10.1161/01.RES.0000162101.76263.8c. Epub 2005 Mar 10.
- Schulze-Bahr E. Short QT syndrome or Andersen syndrome: Yin and Yang of Kir2.1 channel dysfunction. Circ Res. 2005 Apr 15;96(7):703-4. doi: 10.1161/01.RES.0000164186.86838.09. No abstract available.
- Tristani-Firouzi M, Jensen JL, Donaldson MR, Sansone V, Meola G, Hahn A, Bendahhou S, Kwiecinski H, Fidzianska A, Plaster N, Fu YH, Ptacek LJ, Tawil R. Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome). J Clin Invest. 2002 Aug;110(3):381-8. doi: 10.1172/JCI15183.
- Veerapandiyan A, Statland JM, Tawil R. Andersen-Tawil Syndrome. 2004 Nov 22 [updated 2018 Jun 7]. 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/NBK1264/
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