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3. Extracellular modulation of TREK-2 activity with nanobodies provides insight into the mechanisms of K2P channel regulation

4. Gain-of-function mutations in KCNK3 cause a developmental disorder with sleep apnea

6. Ion occupancy of the selectivity filter controls opening of a cytoplasmic gate in the K2P channel TALK-2.

7. Ion occupancy of the selectivity filter controls opening of a cytoplasmic gate in the K2P channel TALK-2

8. Extracellular modulation of TREK-2 activity with nanobodies provides insight into the mechanisms of K2P channel regulation

14. Validation of TREK1 ion channel activators as an immunomodulatory and neuroprotective strategy in neuroinflammation

19. Defective X-gating caused byde novogain-of-function mutations inKCNK3underlies a developmental disorder with sleep apnea

27. Molecular basis of inward rectification: polyamine interaction sites located by combined channel and ligand mutagenesis

28. Functional conversion between A-type and delayed rectifier [K.sup.+] channels by membrane lipids

35. Two functionally distinct subsites for the binding of internal blockers to the pore of voltage-activated K+ channels

36. The inward rectification mechanism of the HERG cardiac potassium channel

38. The molecular basis for an allosteric inhibition of K+-flux gating in K2P channels

39. A pharmacological master key mechanism that unlocks the selectivity filter gate in K + channels

40. A Pharmacological Masterkey Mechanism to Unlock the Selectivity Filter Gate in K+ Channels

41. Gain-of-function mutations in KCNK3cause a developmental disorder with sleep apnea

42. Author response: The molecular basis for an allosteric inhibition of K+-flux gating in K2P channels

43. The VAMP‐associated protein VAPB is required for cardiac and neuronal pacemaker channel function

45. Bilayer-Mediated Structural Transitions Control Mechanosensitivity of the TREK-2 K2P Channel

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