Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Björn C, Knollmann"'
Autor:
Arpita Deb, Brian D. Tow, You Qing, Madelyn Walker, Emmanuel R. Hodges, James A. Stewart, Björn C. Knollmann, Yi Zheng, Ying Wang, Bin Liu
Publikováno v:
Cells, Vol 12, Iss 2, p 204 (2023)
The brief opening mode of the mitochondrial permeability transition pore (mPTP) serves as a calcium (Ca2+) release valve to prevent mitochondrial Ca2+ (mCa2+) overload. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a stress-induced
Externí odkaz:
https://doaj.org/article/f39e521a90294c628983500592008f1a
Autor:
Kyungsoo Kim, Daniel J. Blackwell, Samantha L. Yuen, Madelaine P. Thorpe, Jeffrey N. Johnston, Razvan L. Cornea, Björn C. Knollmann
Publikováno v:
Journal of Molecular and Cellular Cardiology. 180:1-9
Autor:
Andrew E Radbill, Lucy Y Lei, Sachin Y Paranjape, Daniel J Blackwell, Robert L Abraham, Derek S Chew, Satish R Raj, Björn C Knollmann
Publikováno v:
PLoS ONE, Vol 16, Iss 2, p e0246768 (2021)
AimsArrhythmia mechanisms in hypertrophic cardiomyopathy remain uncertain. Preclinical models suggest hypertrophic cardiomyopathy-linked mutations perturb sarcomere length-dependent activation, alter cardiac repolarization in rate-dependent fashion a
Externí odkaz:
https://doaj.org/article/fcae61050cae4e56b6221862325d1ff6
Autor:
Christian L. Egly, Daniel J. Blackwell, Jeffrey Schmeckpeper, Brian P. Delisle, C. David Weaver, Björn C. Knollmann
Publikováno v:
Molecular Pharmacology. 101:236-245
Autor:
Chantal J.M. van Opbergen, Navratan Bagwan, Svetlana R. Maurya, Joon-Chul Kim, Abigail N. Smith, Daniel J. Blackwell, Jeffrey N. Johnston, Björn C. Knollmann, Marina Cerrone, Alicia Lundby, Mario Delmar
Publikováno v:
Circulation
Van Opbergen, C J M, Bagwan, N, Maurya, S R, Kim, J C, Smith, A N, Blackwell, D J, Johnston, J N, Knollmann, B C, Cerrone, M, Lundby, A & Delmar, M 2022, ' Exercise Causes Arrhythmogenic Remodeling of Intracellular Calcium Dynamics in Plakophilin-2-Deficient Hearts ', Circulation, vol. 145, no. 19, pp. 1480-1496 . https://doi.org/10.1161/CIRCULATIONAHA.121.057757
Van Opbergen, C J M, Bagwan, N, Maurya, S R, Kim, J C, Smith, A N, Blackwell, D J, Johnston, J N, Knollmann, B C, Cerrone, M, Lundby, A & Delmar, M 2022, ' Exercise Causes Arrhythmogenic Remodeling of Intracellular Calcium Dynamics in Plakophilin-2-Deficient Hearts ', Circulation, vol. 145, no. 19, pp. 1480-1496 . https://doi.org/10.1161/CIRCULATIONAHA.121.057757
Background: Exercise training, and catecholaminergic stimulation, increase the incidence of arrhythmic events in patients affected with arrhythmogenic right ventricular cardiomyopathy correlated with plakophilin-2 (PKP2) mutations. Separate data show
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1d75342d9dbc919b43db6dae713acc6f
https://europepmc.org/articles/PMC9086182/
https://europepmc.org/articles/PMC9086182/
Autor:
Christian L, Egly, Daniel J, Blackwell, Jeffrey, Schmeckpeper, Brian P, Delisle, C David, Weaver, Björn C, Knollmann
Publikováno v:
Mol Pharmacol
Loss-of-function (LOF) variants in the K(V)11.1 potassium channel cause long QT syndrome (LQTS). Most variants disrupt intracellular channel transport (trafficking) to the cell membrane. Since some channel inhibitors improve trafficking of K(V)11.1 v
Publikováno v:
PLoS ONE, Vol 10, Iss 6, p e0131179 (2015)
Flecainide blocks ryanodine receptor type 2 (RyR2) channels in the open state, suppresses arrhythmogenic Ca2+ waves and prevents catecholaminergic polymorphic ventricular tachycardia (CPVT) in mice and humans. We hypothesized that differences in RyR2
Externí odkaz:
https://doaj.org/article/f3586c3cfcac40768697643738ab6310
Autor:
Christopher N, Johnson, Rekha, Pattanayek, Franck, Potet, Robyn T, Rebbeck, Daniel J, Blackwell, Roman, Nikolaienko, Vasco, Sequeira, Remy, Le Meur, Przemysław B, Radwański, Jonathan P, Davis, Aleksey V, Zima, Razvan L, Cornea, Steven M, Damo, Sandor, Györke, Alfred L, George, Björn C, Knollmann
Publikováno v:
Cell Calcium
Here we report the structure of the widely utilized calmodulin (CaM)-dependent protein kinase II (CaMKII) inhibitor KN93 bound to the Ca(2+)-sensing protein CaM. KN93 is widely believed to inhibit CaMKII by binding to the kinase. The CaM-KN93 interac
Autor:
Karissa M, Dieseldorff Jones, Yeojung, Koh, Rebecca S, Weller, Rajdeep S, Turna, Ferhaan, Ahmad, Sabine, Huke, Björn C, Knollmann, Jose Renato, Pinto, Hyun Seok, Hwang
Publikováno v:
Archives of biochemistry and biophysics. 661
Mutations in cardiac troponin T (TnT) associated with hypertrophic cardiomyopathy generally lead to an increase in the Ca(2+) sensitivity of contraction and susceptibility to arrhythmias. In contrast, TnT mutations linked to dilated cardiomyopathy de