Match!
Nasreen Sultana
Innsbruck Medical University
Cav1.1Skeletal muscleCalciumCalcium channelBiology
5Publications
2H-index
29Citations
What is this?
Publications 5
Newest
#2Nasreen SultanaH-Index: 2
Last. Bernhard E. FlucherH-Index: 37
view all 9 authors...
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 calcium influx through L-type channels (CaV1.1). Using a genetic approach in mice, we demonstrate here that either the L-type calcium currents (LTCCs) or sarcoplasmic reticulum (SR) calcium release is necessary and sufficient to regulate AChR clustering ...
2 CitationsSource
#1Nasreen SultanaH-Index: 2
#2Beatrix Dienes (University of Debrecen)H-Index: 25
Last. Bernhard E. FlucherH-Index: 37
view all 12 authors...
Skeletal muscle excitation-contraction (EC) coupling is independent of calcium influx. In fact alternative splicing of the voltage-gated calcium channel CaV1.1 actively suppresses calcium currents in mature muscle. Whether this is necessary for normal development and function of muscle is not known. However, splicing defects causing aberrant expression of the calcium-conducting developmental CaV1.1e splice variant correlate with muscle weakness in myotonic dystrophy. Here we deleted CaV1.1 exon ...
17 CitationsSource
#1Beatrix Dienes (University of Debrecen)H-Index: 25
#2János Vincze (University of Debrecen)H-Index: 8
Last. László Csernoch (University of Debrecen)H-Index: 28
view all 6 authors...
The adult isoform of voltage-gated L-type calcium channel (CaV1.1a) opens slowly at strong depolarizations, its contribution to the calcium influx during an action potential is negligible in skeletal muscle. In contrast, calcium influx through the embryonic splice variant (CaV1.1e) substantially contributes to depolarization-induced calcium transients as this isoform displays an altered voltage-dependence and gating kinetics as compared to CaV1.1a. Utilizing a genetically modified mouse model (C...
Source
#1Beatrix Dienes (University of Debrecen)H-Index: 25
#2Nasreen Sultana (Innsbruck Medical University)H-Index: 2
Last. László Csernoch (University of Debrecen)H-Index: 28
view all 7 authors...
The embryonic splice variant of the voltage-gated L-type calcium channel (CaV1.1e) displays an altered voltage-dependence and gating kinetics as compared to that expressed in adult skeletal muscle. Because the adult CaV1.1a only opens slowly at strong depolarizations, its contribution as a source of calcium influx during action potentials is negligible. In contrast, calcium influx through the embryonic CaV1.1e substantially contributes to depolarization-induced calcium transients in fetal muscle...
Source
#1Nasreen SultanaH-Index: 2
#2Ariane BenedettiH-Index: 4
Last. Bernhard E. FlucherH-Index: 37
view all 12 authors...
CaV1.1e is the calcium channel splice variant of embryonic skeletal muscle. It functions as voltage sensor in EC coupling, but in contrast to the adult CaV1.1a variant it also supports sizeable calcium currents activating at the same membrane potential as SR calcium release. Mis-splicing of CaV1.1 results in elevated levels of the CaV1.1e variant in mature muscle that correlate with the severity of muscle weakness in patients suffering from dystrophic myotonia. Therefore we hypothesize that excl...
Source
1