All Stories

  1. Sodium-calcium exchangers (NCX): molecular hallmarks underlying the tissue-specific and systemic functions
  2. The C2B Domain Is the Primary Ca2+ Sensor in DOC2B: A Structural and Functional Analysis
  3. Population Shift Underlies Ca2+-induced Regulatory Transitions in the Sodium-Calcium Exchanger (NCX)
  4. NCLX: The mitochondrial sodium calcium exchanger
  5. SK4 Ca 2+ activated K + channel is a critical player in cardiac pacemaker derived from human embryonic stem cells
  6. The SLC8 gene family of sodium–calcium exchangers (NCX) – Structure, function, and regulation in health and disease
  7. Molecular Determinants of Allosteric Regulation in NCX Proteins
  8. The Mitochondrial Na+/Ca2+ Exchanger Upregulates Glucose Dependent Ca2+ Signalling Linked to Insulin Secretion
  9. G503 Is Obligatory for Coupling of Regulatory Domains in NCX Proteins
  10. A Common Ca2+-Driven Interdomain Module Governs Eukaryotic NCX Regulation
  11. Dynamic features of allosteric Ca2+ sensor in tissue-specific NCX variants
  12. A Previously Unrecognized Conductance is a Critical New Player in the Pacemaker of Cardiomyocytes Derived from Human Embryonic Stem Cells
  13. Proton-sensing Ca2+ Binding Domains Regulate the Cardiac Na+/Ca2+ Exchanger
  14. The pH Sensitivity of the Cardiac Na+/Ca2+ Exchanger Depend on Calcium Binding Domains (CBD) of NCX1
  15. Essential Role of the CBD1-CBD2 Linker in Slow Dissociation of Ca2+ from the Regulatory Two-domain Tandem of NCX1
  16. NCLX is an essential component of mitochondrial Na + /Ca 2+ exchange
  17. Kinetic and Equilibrium Properties of Regulatory Calcium Sensors of NCX1 Protein
  18. Direct Loading of the Purified Endogenous Inhibitor into the Cytoplasm of Patched Cardiomyocytes Blocks the Ion Currents and Calcium Transport through the NCX1 Protein
  19. Effects of purified endogenous inhibitor of the Na+/Ca2+ exchanger on ouabain-induced arrhythmias in the atria and ventricle strips of guinea pig
  20. Single α-Domain Constructs of the Na+/Ca2+Exchanger, NCLX, Oligomerize To Form a Functional Exchanger
  21. Purified endogenous inhibitor of the Na/Ca exchanger can enhance the cardiomyocytes contractility and calcium transients
  22. Advanced procedures for separation and analysis of low molecular weight inhibitor (NCXIF) of the cardiac sodium–calcium exchanger
  23. The low molecular weight inhibitor of NCX1 interacts with a cytosolic domain that differs from the ion-transport site of the Na/Ca exchanger
  24. Inotropic and Lusitropic Effects Induced by the Inhibitory Factor of the Na/Ca Exchanger Are Not Mediated by the β-Adrenergic Activation
  25. The endogenous inhibitor of NCX1 does not resemble the properties of digitalis compound
  26. An Unknown Endogenous Inhibitor of Na/Ca Exchange Can Enhance the Cardiac Muscle Contractility
  27. Time-Resolved Monitoring of Electrogenic Na+−Ca2+Exchange in the Isolated Cardiac Sarcolemma Vesicles by Using a Rapid-Response Fluorescent Probe
  28. Actions of myristyl-FRCRCFa, a cell-permeant blocker of the cardiac sarcolemmal Na-Ca exchanger, tested in rabbit ventricular myocytes
  29. Inhibition of the cardiac sarcolemma (cell membrane) Na+-Ca2+ exchanger (NCX1) by peptide based blockers
  30. The peptide ?FRCRCFa", dialysed intracellularly, inhibits the Na/Ca exchange in rabbit ventricular myocytes with high affinity
  31. Kinetics and Mechanism: Modulation of Ion Transport in the Cardiac Sarcolemma Sodium‐Calcium Exchanger by Protons, Monovalent Ions, and Temperatureac
  32. Rapid Interaction of FRCRCFa with the Cytosolic Side of the Cardiac Sarcolemma Na+−Ca2+ Exchanger Blocks the Ion Transport without Preventing the Binding of either Sodium or Calcium
  33. Rate-limiting mechanisms of exchange reactions in the cardiac sarcolemma Na+-Ca2+ exchanger
  34. Positively Charged Cyclic Hexapeptides, Novel Blockers for the Cardiac Sarcolemma Na+-Ca2+ Exchanger
  35. The cardiac sodium-calcium exchanger: Relative rates of calcium and sodium movements and their modulation by protonation-deprotonation of the carrier
  36. Opiates and ?cardioexcitatory? tetrapeptides inhibit sodium-calcium exchange in cardiac sarcolemma vesicles Daniel Khananshvili, Department of Biochemistry, Weizmann Institute of Science, Rehovot 76100, P.O.B. 26, Israel
  37. The effect of opiate agonists and antagonists on Na+-Ca2+ exchange in cardiac sarcolemma vesicles
  38. Mechanism of Partial Reactions in the Cardiac Na+ ‐Ca2+ Exchange Systemaa
  39. Cation antiportes
  40. Distinction between the two basic mechanisms of cation transport in the cardiac sodium-calcium exchange system
  41. The calcium ATPase of sarcoplasmic reticulum is inhibited by one Ca2+ ion
  42. Empirical estimation of interaction energies for ligands binding in the isolated .beta.-subunit of F0F1 ATP synthase from Rhodospirillum rubrum
  43. [53] Selective extraction and reconstitution of F1 subunits from Rhodospirillum rubrum chromatophores
  44. Characterization of an inorganic phosphate binding site on the isolated, reconstitutively active .beta. subunit of F0.cntdot.F1 ATP synthase
  45. Evidence that the Mg-dependent low-affinity binding site for ATP and Pi demonstrated on the isolated beta subunit of the F0.F1 ATP synthase is a catalytic site.
  46. Khananshvili, D. and Z. Gromet‐Elhanan, Demonstration of two binding sites for ADP on the isolated β‐subunit of the Rhodospirillum rubrum RrF0F1‐ATP synthase (1984) FEBS Letters 178, 10‐14
  47. Demonstration of two binding sites for ADP on the isolated β‐subunit of the Rhodospirillum rubrum R1F0F1‐ATP synthase
  48. Characterization of two nucleotide binding sites on the isolated, reconstitutively active .beta. subunit of the F0.cntdot.F1 ATP synthase
  49. Chemical Modification of Essential Amino-Acid Residues in the Chromatophore F1-ATPase and Its Isolated β-Subunit
  50. Modification of histidine residues by diethyl pyrocarbonate leads to inactivation of the Rhodospirillum rubrum RrF1‐ATPase
  51. Chemical modification of the >β-subunit isolated from a membrane-bound Fo·F1-ATP synthase
  52. Sequential removal and reconstitution of subunits β and γ from a membrane-bound Fo·Fl-ATP synthase