Barbara Wardas
Saarland University
Protein subunitBiophysicsGermline mutationCell migrationInositol trisphosphate receptorReceptorCACNA1HChemistryVoltage-dependent calcium channelGatingInositolPrimary aldosteronismFibroblast migrationCancer researchCalcium channelBiology
2Publications
1H-index
9Citations
Publications 3
Newest
#1Alexander Becker (Saarland University)H-Index: 2
#2Barbara Wardas (Saarland University)H-Index: 1
Last. Veit Flockerzi (Saarland University)H-Index: 79
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Voltage-gated Ca2+ (Cav) channels consist of a pore-forming Cavα1 subunit and auxiliary Cavα2-δ and Cavβ subunits. In fibroblasts, Cavβ3, independent of its role as a Cav subunit, reduces the sensitivity to low concentrations of inositol-1,4,5-trisphosphate (IP3). Similarly, Cavβ3 could affect cytosolic [Ca2+] in pancreatic β-cells. Here, we deleted the Cavβ3-encoding gene Cacnb3 in insulin-secreting rat β-(Ins-1) cells using CRISPR/Cas9. These cells were used as controls to investigate the role...
Source
#1Anouar Belkacemi (Saarland University)H-Index: 4
#2Xin Hui (Saarland University)H-Index: 6
Last. Veit Flockerzi (Saarland University)H-Index: 79
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Summary Voltage-gated calcium channels (Cavs) are major Ca 2+ entry pathways in excitable cells. Their β subunits facilitate membrane trafficking of the channel's ion-conducting α1 pore and modulate its gating properties. We report that one β subunit, β3, reduces Ca 2+ release following stimulation of phospholipase C-coupled receptors and inositol 1,4,5-trisphosphate (IP 3 ) formation. This effect requires the SH3-HOOK domain of Cavβ3, includes physical β3/IP 3 receptor interaction, and prevails...
Source
#1Kirsten RoompH-Index: 18
#2Kamil GrzybH-Index: 4
Last. Jochen G. SchneiderH-Index: 32
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