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Decreased inward rectifier potassium current IK1 in dystrophin-deficient ventricular cardiomyocytes.Annexins and membrane fusion.Dynamic interplay of excitatory and inhibitory coupling modes of neuronal L-type calcium channels.Enhanced currents through L-type calcium channels in cardiomyocytes disturb the electrophysiology of the dystrophic heart.Modulation of the heart's electrical properties by the anticonvulsant drug retigabine.δ Subunit-containing GABAA receptors are preferred targets for the centrally acting analgesic flupirtine.Cav 1.3 channels play a crucial role in the formation of paroxysmal depolarization shifts in cultured hippocampal neurons.Cav1.2 and Cav1.3 L-type calcium channels operate in a similar voltage range but show different coupling to Ca(2+)-dependent conductances in hippocampal neurons.Phosphorylation regulates the sensitivity of voltage-gated Kv7.2 channels towards phosphatidylinositol-4,5-bisphosphate.Concomitant facilitation of GABAA receptors and KV7 channels by the non-opioid analgesic flupirtine.Autoregulation in PC12 cells via P2Y receptors: Evidence for non-exocytotic nucleotide release from neuroendocrine cells.Annexin 5 mediates a peroxide-induced Ca(2+) influx in B cells.Inhibition of transmitter release from rat sympathetic neurons via presynaptic M(1) muscarinic acetylcholine receptors.The anticonvulsant retigabine is a subtype selective modulator of GABAA receptors.Raised activity of L-type calcium channels renders neurons prone to form paroxysmal depolarization shifts.P2Y1 receptors mediate an activation of neuronal calcium-dependent K+ channels.Sympathoexcitation by bradykinin involves Ca2+-independent protein kinase C.Calcium current properties in dystrophin-deficient ventricular cardiomyocytes from aged mdx mice.CSTX-1, a toxin from the venom of the hunting spider Cupiennius salei, is a selective blocker of L-type calcium channels in mammalian neurons.Proper Voltage-Dependent Ion Channel Function in Dysferlin-Deficient Cardiomyocytes.Detection Methods for Autoantibodies in Suspected Autoimmune EncephalitisLipid-independent control of endothelial and neuronal TRPC3 channels by lightThe Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and BeyondS-100-immunoreactive protein in Helix neuronsL-type Ca2+ channel-mediated Ca2+ influx adjusts neuronal mitochondrial function to physiological and pathophysiological conditionsThe paroxysmal depolarization shift in epilepsy researchRescue by 4-phenylbutyrate of several misfolded creatine transporter-1 variants linked to the creatine transporter deficiency syndrome
P50
Q33584881-34AD8D1C-C38D-4A27-9C74-D6ACC2FA8502Q33917084-E73814C8-91BD-4BD6-BF1D-5F6B2934CAE3Q34782147-6424B35B-AEDE-408F-9054-EB6A5E6973C3Q36966962-82FC6BE3-E4F8-4602-AE56-6AA0B3466E4FQ38699306-73230B23-0CB2-4B84-80DA-CEE58914F9F0Q38849244-8942A2E0-C4A9-4449-B6FF-FB4FEC9E10D5Q38907067-9A54D907-5F08-440E-A3BA-4CE3670C0E9FQ39204655-990AE605-DC6F-4897-8E43-2E43EE2840E3Q39398244-F9B71FF8-05C2-4700-955F-29FA138E3319Q39424563-1F36958F-689E-41AF-B851-A9863180A5E8Q39959201-E20AB248-14C2-4AC9-90C2-1A34C402DC7AQ40910402-5D9ECC3F-D8A2-4875-8210-08E0E95F72ACQ41425500-AEB73B6B-0AD4-4B82-80DF-8FB0E8B08691Q42212418-4CAA24B6-3034-419B-8937-865A796E28EBQ42536330-ADDE9883-C338-47FD-AC50-9B5B2033E3D8Q42949032-4311A447-8A12-4666-9465-6C2E1F296EB2Q44066986-97F001A6-3E39-4362-BA19-3BFCB6DA1A0DQ50048281-EF76EFDE-0146-4E61-9ADB-5CD4E57A7B15Q52680001-F07AF293-4F1B-444B-840B-3714B38B9293Q53453925-4EF645FF-AED2-45BA-B77C-37C6576F4684Q58576008-14AEF995-D006-4443-8762-C9A984117A70Q64274173-F4DCC7ED-A3EA-4B94-87A4-596643E85F92Q64276838-15D547E7-8875-43E7-BEEB-5856C61474D2Q71646703-061A7E14-E62D-41BF-8123-B6544EA5537AQ89664128-B5D53F18-136A-4588-AF2D-967E9CEF8916Q90586079-657A3891-8A57-454A-BC16-F860043D2603Q92455974-1513459A-C47D-4069-83F3-B9FB9F516F83
P50
description
researcher
@en
name
Helmut Kubista
@en
Kubista H
@nl
type
label
Helmut Kubista
@en
Kubista H
@nl
altLabel
Kubista H
@en
prefLabel
Helmut Kubista
@en
Kubista H
@nl
P106
P31
P496
0000-0002-5805-8649