Zobrazeno 1 - 10
of 79
pro vyhledávání: '"Manfred, Grabner"'
Autor:
Conor McClenaghan, Maya A Mukadam, Jacob Roeglin, Robert C Tryon, Manfred Grabner, Anamika Dayal, Gretchen A Meyer, Colin G Nichols
Publikováno v:
EMBO Molecular Medicine, Vol 15, Iss 6, Pp 1-14 (2023)
Abstract ABCC9‐related intellectual disability and myopathy syndrome (AIMS) arises from loss‐of‐function (LoF) mutations in the ABCC9 gene, which encodes the SUR2 subunit of ATP‐sensitive potassium (KATP) channels. KATP channels are found thr
Externí odkaz:
https://doaj.org/article/5bc13c0117c342b5aab5c020d963a70a
Publikováno v:
eLife, Vol 10 (2021)
Skeletal muscle excitation-contraction (EC) coupling roots in Ca2+-influx-independent inter-channel signaling between the sarcolemmal dihydropyridine receptor (DHPR) and the ryanodine receptor (RyR1) in the sarcoplasmic reticulum. Although DHPR Ca2+
Externí odkaz:
https://doaj.org/article/54751512c56a4f7fb1a69b89d6705b60
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-15 (2019)
The Ca2+-activated Cl- channel TMEM16A/Anoctamin 1 (ANO1) mediates secretion and intestinal motility in gastrointestinal epithelia and smooth muscle cells. Here, the authors show a role for ANO1 in zebrafish skeletal muscle which is activated by SR C
Externí odkaz:
https://doaj.org/article/eecf8fc155dd48389921310afcc01f44
Autor:
Jessica H Myers, Kirsten Denman, Chris DuPont, Ahmed A Hawash, Kevin R Novak, Andrew Koesters, Manfred Grabner, Anamika Dayal, Andrew A Voss, Mark M Rich
Publikováno v:
eLife, Vol 10 (2021)
In addition to the hallmark muscle stiffness, patients with recessive myotonia congenita (Becker disease) experience debilitating bouts of transient weakness that remain poorly understood despite years of study. We performed intracellular recordings
Externí odkaz:
https://doaj.org/article/f201e13c4e5f4c20b08b45b730d90c95
Autor:
Mehmet Mahsum Kaplan, Nasreen Sultana, Ariane Benedetti, Gerald J. Obermair, Nina F. Linde, Symeon Papadopoulos, Anamika Dayal, Manfred Grabner, Bernhard E. Flucher
Publikováno v:
Cell Reports, Vol 23, Iss 13, Pp 3891-3904 (2018)
Summary: Formation of synapses between motor neurons and muscles is initiated by clustering of acetylcholine receptors (AChRs) in the center of muscle fibers prior to nerve arrival. This AChR patterning is considered to be critically dependent on cal
Externí odkaz:
https://doaj.org/article/ca9415eed8b245d291d7bcab970a0a7f
Publikováno v:
Nature Communications, Vol 8, Iss 1, Pp 1-14 (2017)
In mammalian skeletal muscle, the DHPR functions as a voltage sensor to trigger muscle contraction and as a Ca2+ channel. Here the authors show that mice where Ca2+ influx through the DHPR is eliminated display no difference in skeletal muscle functi
Externí odkaz:
https://doaj.org/article/4982215f05324a349f54db466bb3d76c
Publikováno v:
Proceedings of the National Academy of Sciences. 119
Significance Vertebrate skeletal muscle excitation–contraction coupling (ECC) is based on Ca 2+ -influx–independent interchannel cross-talk between DHPR and RyR1. The skeletal muscle DHPR complex consists of the main, voltage-sensing, and pore-fo
Autor:
Kevin R. Novak, Anamika Dayal, Chris DuPont, Jessica H Myers, Mark M. Rich, Andrew Koesters, Kirsten Denman, Andrew A. Voss, Manfred Grabner, Ahmed A. Hawash
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7f6215c5c397370bb10183025c7f0aad
https://doi.org/10.7554/elife.65691.sa2
https://doi.org/10.7554/elife.65691.sa2
Autor:
Chris DuPont, Anamika Dayal, Andrew Koesters, Kevin R. Novak, Kirsten Denman, Andrew A. Voss, Jessica H Myers, Ahmed A. Hawash, Mark M. Rich, Manfred Grabner
Publikováno v:
eLife, Vol 10 (2021)
eLife
eLife
In addition to the hallmark muscle stiffness, patients with recessive myotonia congenita (Becker disease) experience debilitating bouts of transient weakness that remain poorly understood despite years of study. We performed intracellular recordings
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93b40765fcf9a44c20c5417a622d7891
https://doi.org/10.1101/2020.12.23.424129
https://doi.org/10.1101/2020.12.23.424129