kv组合
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Contribution of Kv Channels to Phenotypic Remodeling of Human Uterine Artery Smooth Muscle Cells
Targeted Deletion of Kv4.2 Eliminates Ito,f and Results in Electrical and Molecular Remodeling, With No Evidence of Ventricular Hypertrophy or Myocardial Dysfunction
Stichodactyla helianthus Peptide, a Pharmacological Tool for Studying Kv3.2 Channels
Design of PAP-1, a Selective Small Molecule Kv1.3 Blocker, for the Suppression of Effector Memory T Cells in Autoimmune Diseases
Kv1.5 Surface Expression Is Modulated by Retrograde Trafficking of Newly Endocytosed Channels by the Dynein Motor
The New Anticonvulsant Retigabine Favors Voltage-Dependent Opening of the Kv7.2 (KCNQ2) Channel by Binding to Its Activation Gate
Structural Basis for Competition between Drug Binding and Kv1.3 Accessory Subunit-Induced N-Type Inactivation of Kv1.5 Channels
Investigation of the Phenylalkylamine Binding Site in hKv1.3 (H399T), a Mutant with a Reduced C-Type Inactivated State
Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter
Most LQT2 Mutations Reduce Kv11.1 (hERG) Current by a Class 2 (Trafficking-Deficient) Mechanism
Contribution of Kv Channels to Phenotypic Remodeling of Human Uterine Artery Smooth Muscle Cells
Targeted Deletion of Kv4.2 Eliminates Ito,f and Results in Electrical and Molecular Remodeling, With No Evidence of Ventricular Hypertrophy or Myocardial Dysfunction
Stichodactyla helianthus Peptide, a Pharmacological Tool for Studying Kv3.2 Channels
Design of PAP-1, a Selective Small Molecule Kv1.3 Blocker, for the Suppression of Effector Memory T Cells in Autoimmune Diseases
Kv1.5 Surface Expression Is Modulated by Retrograde Trafficking of Newly Endocytosed Channels by the Dynein Motor
The New Anticonvulsant Retigabine Favors Voltage-Dependent Opening of the Kv7.2 (KCNQ2) Channel by Binding to Its Activation Gate
Structural Basis for Competition between Drug Binding and Kv1.3 Accessory Subunit-Induced N-Type Inactivation of Kv1.5 Channels
Investigation of the Phenylalkylamine Binding Site in hKv1.3 (H399T), a Mutant with a Reduced C-Type Inactivated State
Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter
Most LQT2 Mutations Reduce Kv11.1 (hERG) Current by a Class 2 (Trafficking-Deficient) Mechanism
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