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1. Na+,K+-ATPase with Disrupted Na+ Binding Sites I and III Binds Na+ with Increased Affinity at Site II and Undergoes Na+-Activated Phosphorylation with ATP

2. Molecular cloning and characterization of porcine Na⁺/K⁺-ATPase isoforms α1, α2, α3 and the ATP1A3 promoter.

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3. Role of a conserved ion-binding site tyrosine in ion selectivity of the Na+/K+ pump

4. Cryo-electron microscopy of Na

5. Cryoelectron microscopy of Na

6. Cryoelectron microscopy of Na+,K+-ATPase in the two E2P states with and without cardiotonic steroids

7. Binding of cardiotonic steroids to Na+,K+-ATPase in the E2P state

8. Binding of cardiotonic steroids to Na

9. Disease mutations reveal residues critical to the interaction of P4-ATPases with lipid substrates

10. The α2β2 isoform combination dominates the astrocytic Na+/K+-ATPase activity and is rendered nonfunctional by the α2.G301R familial hemiplegic migraine type 2-associated mutation

11. Distinct effects of Q925 mutation on intracellular and extracellular Na+ and K+ binding to the Na+, K+-ATPase

12. Distinct effects of Q925 mutation on intracellular and extracellular Na

13. Asparagine-905 of the mammalian phospholipid flippase ATP8A2 is essential for lipid substrate-induced activation of ATP8A2 dephosphorylation

14. Neurological disease mutations of α3 Na+,K+-ATPase: Structural and functional perspectives and rescue of compromised function

15. Glutamate transporter activity promotes enhanced Na+/K+-ATPase-mediated extracellular K+management during neuronal activity

16. Functional consequences of the CAPOS mutation E818K of Na+,K+-ATPase

17. Functional consequences of the CAPOS mutation E818K of Na

18. Germline De Novo Mutations in ATP1A1 Cause Renal Hypomagnesemia, Refractory Seizures, and Intellectual Disability

20. The α2β2 isoform combination dominates the astrocytic Na

21. Relationship between Intracellular Na+ Concentration and Reduced Na+ Affinity in Na+,K+-ATPase Mutants Causing Neurological Disease

22. Neurological disease mutations of α3 Na

23. Mania-like behavior induced by genetic dysfunction of the neuron-specific Na + ,K + -ATPase α3 sodium pump

24. The Rapid-onset Dystonia Parkinsonism Mutation D923N of the Na+,K+-ATPase α3 Isoform Disrupts Na+ Interaction at the Third Na+ Site

25. A C-terminal mutation of ATP1A3 underscores the crucial role of sodium affinity in the pathophysiology of rapid-onset dystonia-parkinsonism

26. Crystal Structure of D351A and P312A Mutant Forms of the Mammalian Sarcoplasmic Reticulum Ca2+-ATPase Reveals Key Events in Phosphorylation and Ca2+ Release

29. Importance of a Potential Protein Kinase A Phosphorylation Site of Na+,K+-ATPase and Its Interaction Network for Na+ Binding

30. Specific mutations in mammalian P4-ATPase ATP8A2 catalytic subunit entail differential glycosylation of the accessory CDC50A subunit

32. Mutations Phe785Leu and Thr618Met in Na+,K+-ATPase, Associated with Familial Rapid-onset Dystonia Parkinsonism, Interfere with Na+ Interaction by Distinct Mechanisms

33. Mutation of Gly-94 in transmembrane segment M1 of Na + ,K + -ATPase interferes with Na + and K + binding in E 2 P conformation

34. Interaction between the Catalytic Site and the A-M3 Linker Stabilizes E2/E2P Conformational States of Na+,K+-ATPase

35. Importance of Transmembrane Segment M1 of the Sarcoplasmic Reticulum Ca2+-ATPase in Ca2+ Occlusion and Phosphoenzyme Processing

36. Glutamate-183 in the conserved TGES motif of domain A of sarcoplasmic reticulum Ca 2+ -ATPase assists in catalysis of E 2 / E 2 P partial reactions

37. Dissection of the Functional Differences between Sarco(endo)plasmic Reticulum Ca2+-ATPase (SERCA) 1 and 2 Isoforms and Characterization of Darier Disease (SERCA2) Mutants by Steady-state and Transient Kinetic Analyses

38. Importance of Conserved N-domain Residues Thr441, Glu442, Lys515, Arg560, and Leu562 of Sarcoplasmic Reticulum Ca2+-ATPase for MgATP Binding and Subsequent Catalytic Steps

39. ATP Binding Residues of Sarcoplasmic Reticulum Ca2+-ATPase

40. Importance of Transmembrane Segment M3 of Na+,K+-ATPase for Control of Conformational Changes and the Cytoplasmic Entry Pathway for Na+

41. Importance of Glu282 in Transmembrane Segment M3 of the Na+,K+-ATPase for Control of Cation Interaction and Conformational Changes

42. Rescue of Na+ affinity in aspartate 928 mutants of Na+,K+-ATPase by secondary mutation of glutamate 314

44. Stability cluster links hydrofobic gate to K873 in ATP8A2

45. Darier disease mutation E917K of SERCA2b relieves the inhibitory influence of the 11th transmembrane segment

46. Critical roles of isoleucine-364 and adjacent residues in a hydrophobic gate control of phospholipid transport by the mammalian P4-ATPase ATP8A2

47. Mutation to the Glutamate in the Fourth Membrane Segment of Na+,K+-ATPase and Ca2+-ATPase Affects Cation Binding from Both Sides of the Membrane and Destabilizes the Occluded Enzyme Forms

48. Mutagenesis of Sarcoplasmic Reticulum Ca2+-ATPase

49. Somatic ATP1A1, ATP2B3, and KCNJ5 mutations in aldosterone-producing adenomas

50. Site-Directed Mutagenesis Analysis of the Role of the M5S5 Sector of the Sarcoplasmic Reticulum Ca2+-ATPase