KCNE3

KCNE3
Identifikatori
Aliasi	KCNE3
Vanjski ID-jevi	OMIM: 604433 MGI: 1891124 HomoloGene: 3994 GeneCards: KCNE3
Lokacija gena (čovjek)
Hrom.	Hromosom 11 (čovjek)
Kraj	74,467,729 bp
Lokacija gena (miš)
Hrom.	Hromosom 7 (miš)
Kraj	99,834,076 bp
Obrazac RNK ekspresije
	Više referentnih podataka o ekspresiji
Ontologija gena
Molekularna funkcija	• potassium channel activity; • transmembrane transporter binding; • voltage-gated ion channel activity; • potassium channel regulator activity; • GO:0001948, GO:0016582 vezivanje za proteine; • voltage-gated potassium channel activity; • delayed rectifier potassium channel activity; • voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization;
Ćelijska komponenta	• citoplazma; • integral component of membrane; • Vezikula; • perikaryon; • projekcija ćelije; • membrana; • voltage-gated potassium channel complex; • ćelijska membrana; • neuronal cell body membrane; • dendrit; • Lipidni splav;
Biološki proces	• regulation of potassium ion transport; • positive regulation of voltage-gated calcium channel activity; • regulation of ion transmembrane transport; • ion transport; • potassium ion transport; • potassium ion transmembrane transport; • negative regulation of delayed rectifier potassium channel activity; • regulation of heart rate by cardiac conduction; • negative regulation of potassium ion export across plasma membrane; • negative regulation of voltage-gated potassium channel activity; • negative regulation of membrane repolarization during ventricular cardiac muscle cell action potential; • regulation of ventricular cardiac muscle cell membrane repolarization; • ventricular cardiac muscle cell action potential; • membrane repolarization during action potential; • membrane repolarization during ventricular cardiac muscle cell action potential; • potassium ion export across plasma membrane;
	Izvori:Amigo / QuickGO
Ortolozi
	10008
	57442
	ENSG00000175538
	ENSMUSG00000035165
	Q9Y6H6
	Q9WTW2
	NM_005472
NM_001190869; NM_001190870; NM_001190871; NM_001190950; NM_020574;
	NM_001360466; NM_001360467
	NP_005463
NP_001177798; NP_001177799; NP_001177800; NP_001177879; NP_065599;
	NP_001347395; NP_001347396
	Wikipodaci
Pogledaj/uredi – čovjek	Pogledaj/uredi – miš

Član 3 Isk-srodne porodice kalijskog naponski-vođenog kanala (KCNE3), znan i kao MinK-srodni peptid 2 (MiRP2) jest protein koji je kod ljudi kodiran genom KCNE3 sa hromosoma 11.^[5]^[6]

Aminokiselinska sekvenca uredi

Dužina polipeptidnog lanca je 103 aminokiseline, a molekulska težina 11.710 Da.^[5]

C: Cistein

D: Asparaginska kiselina

E: Glutaminska kiselina

F: Fenilalanin

G: Glicin

H: Histidin

I: Izoleucin

K: Lizin

L: Leucin

M: Metionin

N: Asparagin

P: Prolin

Q: Glutamin

R: Arginin

S: Serin

T: Treonin

V: Valin

W: Triptofan

Y: Tirozin

10	20	30	40	50
METTNGTETW	YESLHAVLKA	LNATLHSNLL	CRPGPGLGPD	NQTEERRASL
PGRDDNSYMY	ILFVMFLFAV	TVGSLILGYT	RSRKVDKRSD	PYHVYIKNRV
SMI

Funkcija uredi

Naponski-vođeni kalijski kanali (K_v) predstavljaju najkompleksniju klasu naponski vođenih ionskih kanala i sa funkcionalnog i sa strukturnog stanovišta. [Njihove različite funkcije uključuju regulaciju oslobađanja neurotransmitera, otkucaja srca, lučenja insulina, ekscitabilnosti neurona, transporta epitelnih elektrolita, kontrakcije glatkih mišića i volumena ćelije. KCNE3 kodira člana petočlane porodice KCNE pomoćnih ili β podjedinica kalijevih (K_v) kanala.

KCNE3 je najpoznatiji po modulaciji α podjedinice KCNQ1 K_v, ali takođe reguliše hERG, K_v2.1, K_v3.x, K_v4.x i K_v12.2 u eksperimentima heterologne koekspresije i/ili in vivo.

Sastavljanje sa KCNE3 pretvara KCNQ1 iz ispravljača naponsko zavisnog odloženog K+ kanala u konstitutivno otvoreni K+ kanal sa skoro linearnim odnosom struja/napon (I/V).^[7] KCNQ1-KCNE3 channels have been detected in the basolateral membrane of mouse small intestinal crypts, where they provide a driving force to regulate Cl- secretion.^[8] Specific amino acids within the transmembrane segment (V72) and extracellular domain (D54 and D55) of KCNE3 are important for its control of KCNQ1 voltage dependence.^[9]^[10] D54 i D55 elektrostatski stupaju u interakciju s R237 u segmentu S4 naponskog senzora KCNQ1, pomažući da se S4 stabilizira u aktiviranom stanju, koji zauzvrat zaključava kanal ako se ćelija ne drži na jako hiperpolarizirajućem (negativnom) membranskom potencijalu. Sposobnost KCNQ1-KCNE3 kanala da ostanu otvoreni pri slabo negativnim membranskim potencijalima dozvoljava njihovu aktivnost u neekscitabilnim, polariziranim epitelnim ćelijama poput onih u crijevima.

KCNE3 također stupa u interakciju sa hERG, a kada se koekspresuje u oocitima Xenopus laevis, KCNE3 inhibira hERG aktivnost nepoznatim mehanizmom. Nije poznato da li se kompleksi hERG-KCNE3 javljaju in vivo.^[7]

KCNE3 stupa u interakciju sa Kv2.1 in vitro i formira komplekse sa njim u srcu i mozgu pacova. KCNE3 usporava aktivaciju i deaktivaciju Kv2.1. KCNE3 također može regulisati kanale podtporodice Kv3, koji su najpoznatiji po tome što dozvoljavaju ultrabrzo pokretanje neurona, zbog izuzetno brzog ulaza (aktivacija i deaktivacija). KCNE3 umjereno usporava aktivaciju i deaktivaciju Kv3.1 i Kv3.2 i umjereno ubrzava njihov C-tip inaktivacije.^[11]^[12] Moguće je da KCNE3 (i KCNE1 i 2) regulacija Kv3.1 i Kv3.2 pomaže da se poveća funkcionalna raznolikost unutar potporodice Kv3.^[13] KCNE3 također reguliše Kv3.4, povećava njegovu struju povećanjem jedinstvene provodljivosti i pomjeranjem ovisnosti napona ulijevo tako da se kanal može otvoriti pri negativnijim naponima. Ovo može omogućiti Kv3.4-KCNE3 kanalima da doprinesu postavljanju potencijala membrane u mirovanju.^[14]

Klinički značaj uredi

Genetički poremećaj gena Kcne3 kod miševa narušava crijevnu cAMP-stimuliranu sekreciju hlorida putem poremećaja crijevnih KCNQ1-KCNE3 kanala koji su važni za regulaciju hloridne struje. KCNE3 također obavlja sličnu funkciju u epitelu mišjih traheja. Delecija Kcne3 kod miševa također predisponira komorskoj aritmogenezi, ali ekspresija KCNE3 nije uočljiva u srcu miševa. Pokazalo se da je mehanizam komorske aritmogeneze indirektan i povezan s autoimunskim napadom nadbubrežne žlijezde i sekundarnim hiperaldosteronizmom (KCNE3 se ne može detektirati u nadbubrežnoj žlijezdi). Povišen aldosteron u serumu predisponira za aritmije izazvane u modelu ishemije/reperfuzijske ozljede ligacije koronarne arterije. Blokada aldosteronskog receptora spironolaktonom uklonila je predispoziciju za komorsku aritmiju kod miševa Kcne3 –/–. Delecija Kcne3 također narušava slušnu funkciju zbog gubitka regulacije Kv4.2 kanala od strane KCNE3 u spiralnim ganglijskim neuronima (SGN) slušnog sistema. Smatra se da KCNE3 reguliše svojstva uključivanja SGN i membranski potencijal , putem svoje modulacije Kv4.2.

Mutacije u ljudskom KCNE3 su povezane sa hipokalemijskom periodičnom paralizom^[5] i Brogadaovim sindromom.^[15]

Povezanost s mutacijom R83H u KCNE3 je kontroverzna i druge grupe su otkrile istu mutaciju kod osoba koje ne pokazuju simptome periodične paralize.^[16] Umjesto toga, mutacija može biti benigni polimorfizam ili zahtijeva još jedan genetički ili ekološki 'hit' prije nego što postane patogena. Kv kanali formirani od Kv3.4 i R83H-KCNE3 imaju oslabljenu funkciju u poređenju sa kanalima divljeg tipa, manje su sposobni da se otvaraju pri negativnim potencijalima i osjetljivi su na protonski blok tokom acidoze.^[14]^[17]

Smatra se da Brugadaov sindrom povezan sa KCNE3 nastaje zato što mutantni KCNE3 nije u stanju da inhibira Kv4.3 kanale u srčanokomorskim miocitima kao što se predlaže kod zdravih osoba. Čini se da se, za razliku od miševa, ekspresija KCNE3 može otkriti u ljudskom srcu. Nije prijavljeno da li ljudi s KCNE3 mutacijama također imaju simptome povezane s nadbubrežnom žlijezdom, kao što je hiperaldosteronizam.

Predloženo je da se mutacije KCNE3 povezuju s Ménièrovom bolešću na japanskom području, stanjem koje se manifestira kao tinitus, spontana vrtoglavica i periodični gubitak sluha,^[18] međutim, ova povezanost je također kontroverzna i nije uočena u populaciji kavkazoida.^[19] U studiji zujanja u ušima koja koristi analizu dubinske sekvencioniranja, autori nisu bili u mogućnosti dokazati ili opovrgnuti povezanost varijacije sekvence KCNE3 sa tinitusom.^[20]

Također pogledajte uredi

Reference uredi

^ ^a ^b ^c GRCh38: Ensembl release 89: ENSG00000175538 - Ensembl, maj 2017
^ ^a ^b ^c GRCm38: Ensembl release 89: ENSMUSG00000035165 - Ensembl, maj 2017
^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ ^a ^b ^c "Entrez Gene: KCNE3 potassium voltage-gated channel, Isk-related family, member 3".
^ Abbott GW, Sesti F, Splawski I, Buck ME, Lehmann MH, Timothy KW, Keating MT, Goldstein SA (Apr 1999). "MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia". Cell. 97 (2): 175–87. doi:10.1016/S0092-8674(00)80728-X. PMID 10219239. S2CID 8507168.
^ ^a ^b Schroeder BC, Waldegger S, Fehr S, Bleich M, Warth R, Greger R, Jentsch TJ (Jan 2000). "A constitutively open potassium channel formed by KCNQ1 and KCNE3". Nature. 403 (6766): 196–9. Bibcode:2000Natur.403..196S. doi:10.1038/35003200. PMID 10646604. S2CID 205004809.
^ Preston P, Wartosch L, Günzel D, Fromm M, Kongsuphol P, Ousingsawat J, Kunzelmann K, Barhanin J, Warth R, Jentsch TJ (Mar 2010). "Disruption of the K+ channel beta-subunit KCNE3 reveals an important role in intestinal and tracheal Cl- transport". The Journal of Biological Chemistry. 285 (10): 7165–75. doi:10.1074/jbc.M109.047829. PMC 2844166. PMID 20051516.
^ Melman YF, Krumerman A, McDonald TV (Jul 2002). "A single transmembrane site in the KCNE-encoded proteins controls the specificity of KvLQT1 channel gating". The Journal of Biological Chemistry. 277 (28): 25187–94. doi:10.1074/jbc.M200564200. PMID 11994278.
^ Choi E, Abbott GW (maj 2010). "A shared mechanism for lipid- and beta-subunit-coordinated stabilization of the activated K+ channel voltage sensor". FASEB Journal. 24 (5): 1518–24. doi:10.1096/fj.09-145219. PMC 2879946. PMID 20040519.
^ McCrossan ZA, Lewis A, Panaghie G, Jordan PN, Christini DJ, Lerner DJ, Abbott GW (Sep 2003). "MinK-related peptide 2 modulates Kv2.1 and Kv3.1 potassium channels in mammalian brain". The Journal of Neuroscience. 23 (22): 8077–91. doi:10.1523/JNEUROSCI.23-22-08077.2003. PMC 6740484. PMID 12954870.
^ McCrossan ZA, Roepke TK, Lewis A, Panaghie G, Abbott GW (Mar 2009). "Regulation of the Kv2.1 potassium channel by MinK and MiRP1". The Journal of Membrane Biology. 228 (1): 1–14. doi:10.1007/s00232-009-9154-8. PMC 2849987. PMID 19219384.
^ Lewis A, McCrossan ZA, Abbott GW (Feb 2004). "MinK, MiRP1, and MiRP2 diversify Kv3.1 and Kv3.2 potassium channel gating". The Journal of Biological Chemistry. 279 (9): 7884–92. doi:10.1074/jbc.M310501200. PMID 14679187.
^ ^a ^b Abbott GW, Butler MH, Bendahhou S, Dalakas MC, Ptacek LJ, Goldstein SA (Jan 2001). "MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis". Cell. 104 (2): 217–31. doi:10.1016/s0092-8674(01)00207-0. PMID 11207363. S2CID 16809594.
^ Delpón E, Cordeiro JM, Núñez L, Thomsen PE, Guerchicoff A, Pollevick GD, Wu Y, Kanters JK, Larsen CT, Hofman-Bang J, Burashnikov E, Christiansen M, Antzelevitch C (Aug 2008). "Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome". Circulation: Arrhythmia and Electrophysiology. 1 (3): 209–18. doi:10.1161/CIRCEP.107.748103. PMC 2585750. PMID 19122847.
^ Sternberg D, Tabti N, Fournier E, Hainque B, Fontaine B (Sep 2003). "Lack of association of the potassium channel-associated peptide MiRP2-R83H variant with periodic paralysis". Neurology. 61 (6): 857–9. doi:10.1212/01.wnl.0000082392.66713.e3. PMID 14504341. S2CID 15449273.
^ Abbott GW, Butler MH, Goldstein SA (Feb 2006). "Phosphorylation and protonation of neighboring MiRP2 sites: function and pathophysiology of MiRP2-Kv3.4 potassium channels in periodic paralysis". FASEB Journal. 20 (2): 293–301. doi:10.1096/fj.05-5070com. PMID 16449802. S2CID 21538479.
^ Doi K, Sato T, Kuramasu T, Hibino H, Kitahara T, Horii A, Matsushiro N, Fuse Y, Kubo T (2005). "Ménière's disease is associated with single nucleotide polymorphisms in the human potassium channel genes, KCNE1 and KCNE3". ORL; Journal for Oto-Rhino-Laryngology and Its Related Specialties. 67 (5): 289–93. doi:10.1159/000089410. PMID 16374062. S2CID 11258678.
^ Campbell CA, Della Santina CC, Meyer NC, Smith NB, Myrie OA, Stone EM, Fukushima K, Califano J, Carey JP, Hansen MR, Gantz BJ, Minor LB, Smith RJ (Jan 2010). "Polymorphisms in KCNE1 or KCNE3 are not associated with Ménière disease in the Caucasian population". American Journal of Medical Genetics Part A. 152A (1): 67–74. doi:10.1002/ajmg.a.33114. PMID 20034061. S2CID 25363712.
^ Sand PG, Langguth B, Kleinjung T (7. 9. 2011). "Deep resequencing of the voltage-gated potassium channel subunit KCNE3 gene in chronic tinnitus". Behavioral and Brain Functions. 7: 39. doi:10.1186/1744-9081-7-39. PMC 3180252. PMID 21899751.

Dopunska literatura uredi

Bonaldo MF, Lennon G, Soares MB (Sep 1996). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Research. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548.
Melman YF, Domènech A, de la Luna S, McDonald TV (Mar 2001). "Structural determinants of K_vLQT1 control by the KCNE family of proteins". The Journal of Biological Chemistry. 276 (9): 6439–44. doi:10.1074/jbc.M010713200. PMID 11104781.
Dedek K, Waldegger S (Sep 2001). "Colocalization of KCNQ1/KCNE channel subunits in the mouse gastrointestinal tract". Pflügers Archiv. 442 (6): 896–902. doi:10.1007/s004240100609. PMID 11680623. S2CID 25496942.
Abbott GW, Goldstein SA (Mar 2002). "Disease-associated mutations in KCNE potassium channel subunits (MiRPs) reveal promiscuous disruption of multiple currents and conservation of mechanism". FASEB Journal. 16 (3): 390–400. doi:10.1096/fj.01-0520hyp. PMID 11874988. S2CID 26205057.
Mazhari R, Nuss HB, Armoundas AA, Winslow RL, Marbán E (Apr 2002). "Ectopic expression of KCNE3 accelerates cardiac repolarization and abbreviates the QT interval". The Journal of Clinical Investigation. 109 (8): 1083–90. doi:10.1172/JCI15062. PMC 150950. PMID 11956246.
Dias Da Silva MR, Cerutti JM, Arnaldi LA, Maciel RM (Nov 2002). "A mutation in the KCNE3 potassium channel gene is associated with susceptibility to thyrotoxic hypokalemic periodic paralysis". The Journal of Clinical Endocrinology and Metabolism. 87 (11): 4881–4. doi:10.1210/jc.2002-020698. PMID 12414843.
Jurkat-Rott K, Lehmann-Horn F (Mar 2004). "Periodic paralysis mutation MiRP2-R83H in controls: Interpretations and general recommendation". Neurology. 62 (6): 1012–5. doi:10.1212/01.wnl.0000119392.29624.88. PMID 15037716. S2CID 16831070.
Lundquist AL, Turner CL, Ballester LY, George AL (Jan 2006). "Expression and transcriptional control of human KCNE genes". Genomics. 87 (1): 119–28. doi:10.1016/j.ygeno.2005.09.004. PMID 16303284.
Panaghie G, Tai KK, Abbott GW (Feb 2006). "Interaction of KCNE subunits with the KCNQ1 K+ channel pore". The Journal of Physiology. 570 (Pt 3): 455–67. doi:10.1113/jphysiol.2005.100644. PMC 1479883. PMID 16308347.
Oh JH, Yang JO, Hahn Y, Kim MR, Byun SS, Jeon YJ, Kim JM, Song KS, Noh SM, Kim S, Yoo HS, Kim YS, Kim NS (Dec 2005). "Transcriptome analysis of human gastric cancer". Mammalian Genome. 16 (12): 942–54. doi:10.1007/s00335-005-0075-2. PMID 16341674. S2CID 69278.

Vanjski linkovi uredi

GeneReviews/NIH/NCBI/UW entry on Brugada syndrome
KCNE3 protein, human na US National Library of Medicine Medical Subject Headings (MeSH)
KCNE3 lokacija ljudskog genoma UCSC Genome Browser.

KCNE3 detalji ljudskog genoma u UCSC Genome Browser.

Q9Y6H6

Ovaj članak uključuje tekst iz Nacionalne medicinske biblioteke Sjedinjenih Država, koji je u javnom vlasništvu.

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000175538 - Ensembl, maj 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000035165 - Ensembl, maj 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[entrez-5] "Entrez Gene: KCNE3 potassium voltage-gated channel, Isk-related family, member 3".

[pmid10219239-6] Abbott GW, Sesti F, Splawski I, Buck ME, Lehmann MH, Timothy KW, Keating MT, Goldstein SA (Apr 1999). "MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia". Cell. 97 (2): 175–87. doi:10.1016/S0092-8674(00)80728-X. PMID 10219239. S2CID 8507168.

[Schroeder-7] Schroeder BC, Waldegger S, Fehr S, Bleich M, Warth R, Greger R, Jentsch TJ (Jan 2000). "A constitutively open potassium channel formed by KCNQ1 and KCNE3". Nature. 403 (6766): 196–9. Bibcode:2000Natur.403..196S. doi:10.1038/35003200. PMID 10646604. S2CID 205004809.

[Preston-8] Preston P, Wartosch L, Günzel D, Fromm M, Kongsuphol P, Ousingsawat J, Kunzelmann K, Barhanin J, Warth R, Jentsch TJ (Mar 2010). "Disruption of the K+ channel beta-subunit KCNE3 reveals an important role in intestinal and tracheal Cl- transport". The Journal of Biological Chemistry. 285 (10): 7165–75. doi:10.1074/jbc.M109.047829. PMC 2844166. PMID 20051516.

[Melman-9] Melman YF, Krumerman A, McDonald TV (Jul 2002). "A single transmembrane site in the KCNE-encoded proteins controls the specificity of KvLQT1 channel gating". The Journal of Biological Chemistry. 277 (28): 25187–94. doi:10.1074/jbc.M200564200. PMID 11994278.

[Choi-10] Choi E, Abbott GW (maj 2010). "A shared mechanism for lipid- and beta-subunit-coordinated stabilization of the activated K+ channel voltage sensor". FASEB Journal. 24 (5): 1518–24. doi:10.1096/fj.09-145219. PMC 2879946. PMID 20040519.

[McCrossan_brain-11] McCrossan ZA, Lewis A, Panaghie G, Jordan PN, Christini DJ, Lerner DJ, Abbott GW (Sep 2003). "MinK-related peptide 2 modulates Kv2.1 and Kv3.1 potassium channels in mammalian brain". The Journal of Neuroscience. 23 (22): 8077–91. doi:10.1523/JNEUROSCI.23-22-08077.2003. PMC 6740484. PMID 12954870.

[McCrossan_heart-12] McCrossan ZA, Roepke TK, Lewis A, Panaghie G, Abbott GW (Mar 2009). "Regulation of the Kv2.1 potassium channel by MinK and MiRP1". The Journal of Membrane Biology. 228 (1): 1–14. doi:10.1007/s00232-009-9154-8. PMC 2849987. PMID 19219384.

[Lewis-13] Lewis A, McCrossan ZA, Abbott GW (Feb 2004). "MinK, MiRP1, and MiRP2 diversify Kv3.1 and Kv3.2 potassium channel gating". The Journal of Biological Chemistry. 279 (9): 7884–92. doi:10.1074/jbc.M310501200. PMID 14679187.

[Abbott_Cell_2-14] Abbott GW, Butler MH, Bendahhou S, Dalakas MC, Ptacek LJ, Goldstein SA (Jan 2001). "MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis". Cell. 104 (2): 217–31. doi:10.1016/s0092-8674(01)00207-0. PMID 11207363. S2CID 16809594.

[pmid19122847-15] Delpón E, Cordeiro JM, Núñez L, Thomsen PE, Guerchicoff A, Pollevick GD, Wu Y, Kanters JK, Larsen CT, Hofman-Bang J, Burashnikov E, Christiansen M, Antzelevitch C (Aug 2008). "Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome". Circulation: Arrhythmia and Electrophysiology. 1 (3): 209–18. doi:10.1161/CIRCEP.107.748103. PMC 2585750. PMID 19122847.

[16] Sternberg D, Tabti N, Fournier E, Hainque B, Fontaine B (Sep 2003). "Lack of association of the potassium channel-associated peptide MiRP2-R83H variant with periodic paralysis". Neurology. 61 (6): 857–9. doi:10.1212/01.wnl.0000082392.66713.e3. PMID 14504341. S2CID 15449273.

[17] Abbott GW, Butler MH, Goldstein SA (Feb 2006). "Phosphorylation and protonation of neighboring MiRP2 sites: function and pathophysiology of MiRP2-Kv3.4 potassium channels in periodic paralysis". FASEB Journal. 20 (2): 293–301. doi:10.1096/fj.05-5070com. PMID 16449802. S2CID 21538479.

[18] Doi K, Sato T, Kuramasu T, Hibino H, Kitahara T, Horii A, Matsushiro N, Fuse Y, Kubo T (2005). "Ménière's disease is associated with single nucleotide polymorphisms in the human potassium channel genes, KCNE1 and KCNE3". ORL; Journal for Oto-Rhino-Laryngology and Its Related Specialties. 67 (5): 289–93. doi:10.1159/000089410. PMID 16374062. S2CID 11258678.

[19] Campbell CA, Della Santina CC, Meyer NC, Smith NB, Myrie OA, Stone EM, Fukushima K, Califano J, Carey JP, Hansen MR, Gantz BJ, Minor LB, Smith RJ (Jan 2010). "Polymorphisms in KCNE1 or KCNE3 are not associated with Ménière disease in the Caucasian population". American Journal of Medical Genetics Part A. 152A (1): 67–74. doi:10.1002/ajmg.a.33114. PMID 20034061. S2CID 25363712.

[20] Sand PG, Langguth B, Kleinjung T (7. 9. 2011). "Deep resequencing of the voltage-gated potassium channel subunit KCNE3 gene in chronic tinnitus". Behavioral and Brain Functions. 7: 39. doi:10.1186/1744-9081-7-39. PMC 3180252. PMID 21899751.

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