Philippe Lory, Ph.D.

Affiliations: 
Département de Physiologie CNRS, Montpellier, Montpellier, Occitanie, France 
Area:
ion channels
Website:
http://www.igf.cnrs.fr/
Google:
"Philippe Lory"
Mean distance: 17.35 (cluster 28)
 
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Publications

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Qebibo L, Davakan A, Nesson-Dauphin M, et al. (2024) The characterization of new de novo CACNA1G variants affecting the intracellular gate of Cav3.1 channel broadens the spectrum of neurodevelopmental phenotypes in SCA42ND. Genetics in Medicine : Official Journal of the American College of Medical Genetics. 101337
Huang J, Fan X, Jin X, et al. (2024) Structural basis for human Ca3.2 inhibition by selective antagonists. Cell Research
Lory P. (2024) The good company of T-type calcium channels : Commentary on: "T-type calcium channelosome," a review by N. Weiss and G. W. Zamponi. Pflugers Archiv : European Journal of Physiology. 476: 149-150
Monteil A, Guérineau NC, Gil-Nagel A, et al. (2023) New insights into the physiology and pathophysiology of the atypical sodium leak channel NALCN. Physiological Reviews
Nicole S, Lory P. (2021) New Challenges Resulting From the Loss of Function of Na1.4 in Neuromuscular Diseases. Frontiers in Pharmacology. 12: 751095
Guérineau NC, Monteil A, Lory P. (2021) Sodium background currents in endocrine/neuroendocrine cells: Towards unraveling channel identity and contribution in hormone secretion. Frontiers in Neuroendocrinology. 63: 100947
Lory P, Nicole S, Monteil A. (2020) Neuronal Cav3 channelopathies: recent progress and perspectives. Pflugers Archiv : European Journal of Physiology. 472: 831-844
Chemin J, Stamenic TT, Cazade M, et al. (2019) A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type Ca channels. Scientific Reports. 9: 15642
Bouasse M, Impheng H, Servant Z, et al. (2019) Functional expression of CLIFAHDD and IHPRF pathogenic variants of the NALCN channel in neuronal cells reveals both gain- and loss-of-function properties. Scientific Reports. 9: 11791
Chemin J, Siquier-Pernet K, Nicouleau M, et al. (2018) De novo mutation screening in childhood-onset cerebellar atrophy identifies gain-of-function mutations in the CACNA1G calcium channel gene. Brain : a Journal of Neurology
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