Donnerstag, 09. November 2017, 17:00 - 18:00 iCal
Guest Lecture by Philippe LORY, PhD
Functional modeling of human calcium channelopathies
UZA 2, Hörsaal 6/Lecture Hall 6
Althanstraße 14, Pharmaziegebäude, 1090 Vienna
Lecture
The Doctoral Program ION CHANNELS AND TRANSPORTERS AS MOLECULAR DRUG TARGETS („MolTag“) is pleased to invite you to the following lecture
Functional modeling of human calcium channelopathies
by Philippe LORY, PhD
Institut de Génomique Fonctionnelle (IGF), Neuroscience & Ion Channel Biology Dept. ,CNRS - INSERM – Univ. de Montpellier
on: Thursday, November 9th 2017, 05:00 pm (17:00 Uhr)
at: UZA 2, Althanstr. 14, 1090 Vienna, LECTURE HALL 6
Biosketch - Trained in electrophysiology, Philippe Lory is now leading the team ‘Ion Channels in Neuronal Excitability and Diseases’ at IGF, Montpellier. His expertise covers ion channel physiology, regulation and channelopathies, especially for voltage-gated calcium channels. Calcium channelopathies include forms of epilepsy, migraine, ataxia, neuropathic pain and autism. His lab investigates the pathogenic mechanisms underlying these calcium channelopathies and decipher how these channels are regulated for their physiological activity.
Selected publications : Vitko et al (2007). J Neurosci. 27(2):322-30.Mezghrani et al (2008) J Neurosci. 28(17):4501-11; Blesneac et al (2015) PNAS Nov 3;112(44):13705-10.; Coutelier et al (2016) Am J Hum Genet. Nov 5;97(5):726-37. Voisin et al J Physiol. 2016 Jul 1;594(13):3561-74; Daniil et al (2016 EBioMedicine. S2352-3964(16)30457-1.; Cazade et al (2017) eLife 10.7554/eLife.22331; Dorgans et al (2017) Neurobiol Dis. Oct;106:110-123
Abstract: These last years, our group has contributed to the characterization of several calcium channel mutations linked to neurological diseases in humans. The talk will present how we investigate the pathogenic mechanisms underlying channelopathies, especially for new mutations recently discovered. Importantly, such studies provide in turn new clues to identify how these channels are regulated and contribute to physiology.
Some recent publications of the lab on this topic (4): Dorgans K, Salvi J, Bertaso F, Bernard L, Lory P, Doussau F, Mezghrani A. (2017). Characterization of the dominant inheritance mechanism of Episodic Ataxia type 2. Neurobiol Dis. 106:110-123.
Daniil G, Fernandes-Rosa FL, Chemin J, Blesneac I, Beltrand J, Polak M, Jeunemaitre X, Boulkroun S, Amar L, Strom TM, Lory P, Zennaro MC. (2016). CACNA1H Mutations Are Associated With Different Forms of Primary Aldosteronism. EBioMedicine. 13:225-236.
Coutelier M, Blesneac I, Monteil A, Monin ML, Ando K, Mundwiller E, Brusco A, Le Ber I, Anheim M, Castrioto A, Duyckaerts C, Brice A, Durr A, Lory P, Stevanin G. (2015). A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia. Am J Hum Genet. 97(5):726-37.
Salvi J, Bertaso F, Mausset-Bonnefont AL, Metz A, Lemmers C, Ango F, Fagni L, Lory P, Mezghrani A. (2014). RNAi silencing of P/Q-type calcium channels in Purkinje neurons of adult mouse leads to episodic ataxia type 2. Neurobiol Dis. 68:47-56.
Zur Webseite der Veranstaltung
Veranstalter
Doktoratskolleg "Molecular Drug Targets"
Kontakt
Susanne Menschik-Zunzer
Department of Pharmacology and Toxicology, UZA 2
DK Molecular Drug Targets
01 4277 55320
susanne.menschik-zunzer@univie.ac.at, office.moltag@univie.ac.at
Erstellt am Donnerstag, 12. Oktober 2017, 10:52
Letzte Änderung am Montag, 16. Oktober 2017, 09:41