97 results on '"BIDAUD, I"'
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2. The increase of extracellular Ca2+ from physiological concentrations to hypercalcemia impairs sino-atrial automaticity
3. Cholinergic regulation of cardiac pacemaker activity by L-type Cav1.3 channels
4. Autonomous initiation of pacemaking by L-type Cav1.3 calcium channels in mouse sino-atrial myocytes
5. L-type Cav1.3 calcium channels are key actors in beta-adrenergic triggered automaticity in dormant mouse sino-atrial myocytes
6. P666Heart rate control protects against ischemia-reperfusion injury
7. Cholinergic regulation of cardiac pacemaker activity by l-type cav1.3 channels
8. Hypercalcemia impairs sino-atrial automaticity through excessive Cav1.2-mediated Ca2+ influx
9. Cholinergic regulation of heart rate: Functional importance of l-type cav1.3 channels
10. Genetic ablation of G protein-gated inwardly rectifying K+ (Girk)4 channels prevents heart rate reduction induced by intensive exercise training
11. Autonomous initiation of pacemaking by L-type Cav1.3 calcium channels in mouse sino-atrial myocytes
12. The T-type Calcium Channel Mutations Associated with Childhood Absence Epilepsy Increase Plasma Membrane Expression: 038
13. In Situ Hybridization Localization of TRH Precursor and TRH Receptor mRNAs in the Brain and Pituitary of Xenopus laevis
14. Mitochondria and L-Type Ca2+ channels interplay in the regulation of Ca2+ dynamics in murine pacemaker cells
15. Role of L-type Cav1.3 Ca2+ channels in Ca2+ handling and SAN pacemaker activity altered by external conditions
16. Heart automaticity in mice lacking L-type Cav1.3 and T-type Cav3.1 Ca2+ channels: Insights into the cardiac pacemaker mechanism
17. Inhibition of KACh channels by the bee venom peptide tertiapin-Q rescues inherited cardiac conduction defects and sino-atrial bradycardia and atrioventricular block in models of congenital dysfunction
18. P1083Heart automaticity in mice lacking pacemaker L-type Cav1.3 and T-type Cav3.1 channels
19. 55Role of L-type Cav1.3 Ca2+ channels in Ca2+ handling and sinoatrial node pacemaker activity altered by external conditions
20. Heart automaticity in mice lacking “pacemaker” L-type Ca v 1.3 and Ttype Ca v 3.1 channels
21. Concurrent genetic or pharmacologic targeting of L-type Ca 2+ Ca v 1.3 and ‘funny’ f-(HCN) channels eliminates the ‘fight-or-flight’ response in sino-atrial pacemaker activity
22. Inhibition of K ACh channels by the bee venom peptide tertiapin-Q rescues sino-atrial bradycardia and atrioventricular block in models of congenital sino-atrial dysfunction
23. L-type Cav1.3 and T-type Cav3.1 calcium channels in cardiac pacemaker activity
24. In Situ Hybridization Localization of TRH Precursor and TRH Receptor mRNAs in the Brain and Pituitary of Xenopus laevis
25. Distribution of the mRNAs encoding the thyrotropin-releasing hormone (TRH) precursor and three TRH receptors in the brain and pituitary of Xenopus laevis: Effect of background color adaptation on TRH and TRH receptor gene expression
26. The I-II Loop Controls Plasma Membrane Expression and Gating of Cav3.2 T-Type Ca2+ Channels: A Paradigm for Childhood Absence Epilepsy Mutations
27. T-type calcium channels in differentiation and proliferation
28. In SituHybridization Localization of TRH Precursor and TRH Receptor mRNAs in the Brain and Pituitary ofXenopus laevis
29. 069 - Concurrent genetic or pharmacologic targeting of L-type Ca2+ Cav1.3 and ‘funny’ f-(HCN) channels eliminates the ‘fight-or-flight’ response in sino-atrial pacemaker activity.
30. 157 - Heart automaticity in mice lacking “pacemaker” L-type Cav1.3 and Ttype Cav3.1 channels.
31. 220 - Inhibition of KACh channels by the bee venom peptide tertiapin-Q rescues sino-atrial bradycardia and atrioventricular block in models of congenital sino-atrial dysfunction.
32. 607 - L-type Cav1.3 and T-type Cav3.1 calcium channels in cardiac pacemaker activity.
33. P666 Heart rate control protects against ischemia-reperfusion injury.
34. Selective blockade of Ca v 1.2 (α1C) versus Ca v 1.3 (α1D) L-type calcium channels by the black mamba toxin calciseptine.
35. Heart rate reduction after genetic ablation of L-type Ca v 1.3 channels induces cardioprotection against ischemia-reperfusion injury.
36. L-Type Ca v 1.3 Calcium Channels Are Required for Beta-Adrenergic Triggered Automaticity in Dormant Mouse Sinoatrial Pacemaker Cells.
37. The funny current in genetically modified mice.
38. Intrinsic Electrical Remodeling Underlies Atrioventricular Block in Athletes.
39. Genetic Ablation of G Protein-Gated Inwardly Rectifying K + Channels Prevents Training-Induced Sinus Bradycardia.
40. Pharmacologic Approach to Sinoatrial Node Dysfunction.
41. Concomitant genetic ablation of L-type Ca v 1.3 (α 1D ) and T-type Ca v 3.1 (α 1G ) Ca 2+ channels disrupts heart automaticity.
42. Maurocalcin and its analog MCaE12A facilitate Ca2+ mobilization in cardiomyocytes.
43. Correction to: Channelopathies of voltage-gated L-type Cav1.3/α 1D and T-type Cav3.1/α 1G Ca 2+ channels in dysfunction of heart automaticity.
44. Channelopathies of voltage-gated L-type Cav1.3/α 1D and T-type Cav3.1/α 1G Ca 2+ channels in dysfunction of heart automaticity.
45. Inhibition of G protein-gated K + channels by tertiapin-Q rescues sinus node dysfunction and atrioventricular conduction in mouse models of primary bradycardia.
46. Clock-dependent and system-driven oscillators interact in the suprachiasmatic nuclei to pace mammalian circadian rhythms.
47. Activity-dependent regulation of T-type calcium channels by submembrane calcium ions.
48. Rescuing cardiac automaticity in L-type Cav1.3 channelopathies and beyond.
49. G protein-gated IKACh channels as therapeutic targets for treatment of sick sinus syndrome and heart block.
50. Phosphorylation of the Cav3.2 T-type calcium channel directly regulates its gating properties.
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