Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Jan, Pawlowitz"'
Autor:
Sören Brandenburg, Jan Pawlowitz, Vanessa Steckmeister, Hariharan Subramanian, Dennis Uhlenkamp, Marina Scardigli, Mufassra Mushtaq, Saskia I. Amlaz, Tobias Kohl, Jörg W. Wegener, Demetrios A. Arvanitis, Despina Sanoudou, Leonardo Sacconi, Gerd Hasenfuß, Niels Voigt, Viacheslav O. Nikolaev, Stephan E. Lehnart
Publikováno v:
Journal of Molecular and Cellular Cardiology. 165:141-157
Autor:
Sören Brandenburg, Jan Pawlowitz, Funsho E. Fakuade, Daniel Kownatzki-Danger, Tobias Kohl, Gyuzel Y. Mitronova, Marina Scardigli, Jakob Neef, Constanze Schmidt, Felix Wiedmann, Francesco S. Pavone, Leonardo Sacconi, Ingo Kutschka, Samuel Sossalla, Tobias Moser, Niels Voigt, Stephan E. Lehnart
Publikováno v:
Frontiers in Physiology, Vol 9 (2018)
Rationale: Recently, abundant axial tubule (AT) membrane structures were identified deep inside atrial myocytes (AMs). Upon excitation, ATs rapidly activate intracellular Ca2+ release and sarcomeric contraction through extensive AT junctions, a cell-
Externí odkaz:
https://doaj.org/article/a7e5511ae07e47db91b405f3d2b0cd8e
Autor:
Sören, Brandenburg, Jan, Pawlowitz, Vanessa, Steckmeister, Hariharan, Subramanian, Dennis, Uhlenkamp, Marina, Scardigli, Mufassra, Mushtaq, Saskia I, Amlaz, Tobias, Kohl, Jörg W, Wegener, Demetrios A, Arvanitis, Despina, Sanoudou, Leonardo, Sacconi, Gerd, Hasenfuß, Niels, Voigt, Viacheslav O, Nikolaev, Stephan E, Lehnart
Publikováno v:
Journal of molecular and cellular cardiology. 165
Axial tubule junctions with the sarcoplasmic reticulum control the rapid intracellular Ca
Autor:
Stephan E. Lehnart, Jonas Peper, Gyuzel Yu. Mitronova, Xander H.T. Wehrens, Tobias Kohl, Eva A. Rog-Zielinska, Jan Pawlowitz, Gerd Hasenfuss, Samuel Sossalla, Benjamin Eikenbusch, Peter Kohl, Sören Brandenburg
Publikováno v:
JCI Insight. 4
Atrial dysfunction is highly prevalent and associated with increased severity of heart failure. While rapid excitation-contraction coupling depends on axial junctions in atrial myocytes, the molecular basis of atrial loss of function remains unclear.