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Bernd Fakler

Researcher at University of Tübingen

Publications -  47
Citations -  4809

Bernd Fakler is an academic researcher from University of Tübingen. The author has contributed to research in topics: Gating & Inward-rectifier potassium ion channel. The author has an hindex of 31, co-authored 47 publications receiving 4672 citations. Previous affiliations of Bernd Fakler include University of Zurich & University of Oxford.

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Mechanism of calcium gating in small-conductance calcium-activated potassium channels

TL;DR: The mechanism of calcium gating is studied and it is found that small-conductance calcium-activated potassium channels are not gated by calcium binding directly to the channel α-subunits, instead, the functional SK channels are heteromeric complexes with calmodulin, which is constitutively associated with the α- subunits in a calcium-independent manner.
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PIP2 and PIP as Determinants for ATP Inhibition of KATP Channels

TL;DR: It is reported here that phosphatidylinositol-4, 5-bisphosphate (PIP2) and phosphorus-4-phosphates(PIP) controlled ATP inhibition of cloned KATP channels (Kir6.2 and SUR1) and represents a mechanism for control of excitability through phospholipids.
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Intracellular anions as the voltage sensor of prestin, the outer hair cell motor protein

TL;DR: It is shown that voltage sensitivity is conferred to prestin by the intracellular anions chloride and bicarbonate, which support a model in which anions act as extrinsic voltage sensors, which bind to the prestin molecule and thus trigger the conformational changes required for motility of OHCs.
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Strong voltage-dependent inward rectification of inward rectifier K+ channels is caused by intracellular spermine

TL;DR: It is shown that strong voltage dependence of rectification found under physiological conditions is predominantly due to the effect of intracellular spermine.
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Gating of Ca2+-activated K+ channels controls fast inhibitory synaptic transmission at auditory outer hair cells.

TL;DR: It is shown here that unitary inhibitory postsynaptic currents at this synapse are mediated by SK2 channels and occur rapidly, with rise and decay time constants of approximately 6 ms and approximately 30 ms, respectively.