Bernard Attali

Affiliations: 
Neurobiology Weizmann Institute of Science, Rehovot, Israel 
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"Bernard Attali"
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Lipinsky M, Tobelaim WS, Peretz A, et al. (2020) A unique mechanism of inactivation gating of the Kv channel family member Kv7.1 and its modulation by PIP2 and calmodulin. Science Advances. 6
Lezmy J, Gelman H, Katsenelson M, et al. (2020) M-current inhibition in hippocampal excitatory neurons triggers intrinsic and synaptic homeostatic responses at different temporal scales. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience
Attali B, Lezmy J, Katsenelson M, et al. (2020) M-Current Inhibition in Hippocampal Neurons Triggers Intrinsic and Synaptic Homeostatic Responses at Different Temporal Scales Biophysical Journal. 118
Bueno-Levy H, Weisbrod D, Yadin D, et al. (2019) The Hyperpolarization-Activated Cyclic-Nucleotide-Gated Channel Blocker Ivabradine Does Not Prevent Arrhythmias in Catecholaminergic Polymorphic Ventricular Tachycardia. Frontiers in Pharmacology. 10: 1566
Meisel E, Tobelaim W, Dvir M, et al. (2018) Inactivation gating of Kv7.1 channels does not involve concerted cooperative subunit interactions. Channels (Austin, Tex.). 12: 89-99
Lezmy J, Lipinsky M, Khrapunsky Y, et al. (2017) M-current inhibition rapidly induces a unique CK2-dependent plasticity of the axon initial segment. Proceedings of the National Academy of Sciences of the United States of America. 114: E10234-E10243
Tobelaim WS, Dvir M, Lebel G, et al. (2017) Ca(2+)-Calmodulin and PIP2 interactions at the proximal C-terminus of Kv7 channels. Channels (Austin, Tex.). 0
Haron-Khun S, Weisbrod D, Bueno H, et al. (2017) SK4 K(+) channels are therapeutic targets for the treatment of cardiac arrhythmias. Embo Molecular Medicine
Tobelaim WS, Dvir M, Lebel G, et al. (2017) Competition of calcified calmodulin N lobe and PIP2 to an LQT mutation site in Kv7.1 channel. Proceedings of the National Academy of Sciences of the United States of America
Patrich E, Piontkewitz Y, Peretz A, et al. (2016) Maternal immune activation produces neonatal excitability defects in offspring hippocampal neurons from pregnant rats treated with poly I:C. Scientific Reports. 6: 19106
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