These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
7. Gain-of-function mutations in the calcium channel CACNA1C (Cav1.2) cause non-syndromic long-QT but not Timothy syndrome. Wemhöner K; Friedrich C; Stallmeyer B; Coffey AJ; Grace A; Zumhagen S; Seebohm G; Ortiz-Bonnin B; Rinné S; Sachse FB; Schulze-Bahr E; Decher N J Mol Cell Cardiol; 2015 Mar; 80():186-95. PubMed ID: 25633834 [TBL] [Abstract][Full Text] [Related]
8. Intersegment contacts determine geometry of the open and closed states in P-loop channels. Tikhonov DB; Zhorov BS J Biomol Struct Dyn; 2020 Mar; 38(4):1012-1027. PubMed ID: 30963813 [TBL] [Abstract][Full Text] [Related]
9. Ion-pair interactions between voltage-sensing domain IV and pore domain I regulate Ca El Ghaleb Y; Fernández-Quintero ML; Monteleone S; Tuluc P; Campiglio M; Liedl KR; Flucher BE Biophys J; 2021 Oct; 120(20):4429-4441. PubMed ID: 34506774 [TBL] [Abstract][Full Text] [Related]
10. The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels. Barrett CF; Tsien RW Proc Natl Acad Sci U S A; 2008 Feb; 105(6):2157-62. PubMed ID: 18250309 [TBL] [Abstract][Full Text] [Related]
11. CaV1.2 channelopathic mutations evoke diverse pathophysiological mechanisms. Bamgboye MA; Herold KG; Vieira DCO; Traficante MK; Rogers PJ; Ben-Johny M; Dick IE J Gen Physiol; 2022 Nov; 154(11):. PubMed ID: 36167061 [TBL] [Abstract][Full Text] [Related]
12. Timothy mutation disrupts the link between activation and inactivation in Ca(V)1.2 protein. Depil K; Beyl S; Stary-Weinzinger A; Hohaus A; Timin E; Hering S J Biol Chem; 2011 Sep; 286(36):31557-64. PubMed ID: 21685391 [TBL] [Abstract][Full Text] [Related]
13. Conformational changes of an ion-channel during gating and emerging electrophysiologic properties: Application of a computational approach to cardiac Kv7.1. Nekouzadeh A; Rudy Y Prog Biophys Mol Biol; 2016 Jan; 120(1-3):18-27. PubMed ID: 26743208 [TBL] [Abstract][Full Text] [Related]
14. Arrhythmogenesis in Timothy Syndrome is associated with defects in Ca(2+)-dependent inactivation. Dick IE; Joshi-Mukherjee R; Yang W; Yue DT Nat Commun; 2016 Jan; 7():10370. PubMed ID: 26822303 [TBL] [Abstract][Full Text] [Related]
15. State-dependent inter-repeat contacts of exceptionally conserved asparagines in the inner helices of sodium and calcium channels. Tikhonov DB; Bruhova I; Garden DP; Zhorov BS Pflugers Arch; 2015 Feb; 467(2):253-66. PubMed ID: 24728659 [TBL] [Abstract][Full Text] [Related]
17. Mutation of colocalized residues of the pore helix and transmembrane segments S5 and S6 disrupt deactivation and modify inactivation of KCNQ1 K+ channels. Seebohm G; Westenskow P; Lang F; Sanguinetti MC J Physiol; 2005 Mar; 563(Pt 2):359-68. PubMed ID: 15649981 [TBL] [Abstract][Full Text] [Related]
18. Calcineurin Controls Voltage-Dependent-Inactivation (VDI) of the Normal and Timothy Cardiac Channels. Cohen-Kutner M; Yahalom Y; Trus M; Atlas D Sci Rep; 2012; 2():366. PubMed ID: 22511998 [TBL] [Abstract][Full Text] [Related]
19. CaV1.2 channelopathies: from arrhythmias to autism, bipolar disorder, and immunodeficiency. Liao P; Soong TW Pflugers Arch; 2010 Jul; 460(2):353-9. PubMed ID: 19916019 [TBL] [Abstract][Full Text] [Related]
20. Contribution of S4 segments and S4-S5 linkers to the low-voltage activation properties of T-type CaV3.3 channels. Sanchez-Sandoval AL; Herrera Carrillo Z; Díaz Velásquez CE; Delgadillo DM; Rivera HM; Gomora JC PLoS One; 2018; 13(2):e0193490. PubMed ID: 29474447 [TBL] [Abstract][Full Text] [Related] [Next] [New Search]