Philippe Lory相关文献与解析，生知库 | 链接生命科学的每一步

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

钠离子背景电导控制着小鼠肾上腺嗜铬细胞在原位的放电模式。

Alexandre Milman ,Stéphanie Ventéo ,Jean-Louis Bossu ,Pierre Fontanaud ,Arnaud Monteil ,Philippe Lory ,Nathalie C Guérineau

细胞生物学

免疫/内分泌

发表日期：2021

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A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type Ca2+ channels

一种新的磷酸调节机制有助于 T 型 Ca2+ 通道的钙依赖性调节

期刊:Scientific Reports

影响因子:3.8

doi:10.1038/s41598-019-52194-6

Jean Chemin, Tamara Timic Stamenic, Magalie Cazade, Jodie Llinares, Iulia Blesneac, Slobodan M Todorovic, Philippe Lory

发表日期：2019

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Functional expression of CLIFAHDD and IHPRF pathogenic variants of the NALCN channel in neuronal cells reveals both gain- and loss-of-function properties

神经元细胞中 NALCN 通道 CLIFAHDD 和 IHPRF 致病变异的功能性表达揭示了功能获得和功能丧失的特性

期刊:Scientific Reports

影响因子:3.8

doi:10.1038/s41598-019-48071-x

Malik Bouasse, Hathaichanok Impheng, Zoe Servant, Philippe Lory, Arnaud Monteil

Lysosomal and network alterations in human mucopolysaccharidosis type VII iPSC-derived neurons

人类粘多糖贮积症 VII 型 iPSC 衍生神经元中的溶酶体和网络改变

期刊:Scientific Reports

影响因子:3.8

doi:10.1038/s41598-018-34523-3

Neus Bayó-Puxan, Ana Paula Terrasso, Sophie Creyssels, Daniel Simão, Christina Begon-Pescia, Marina Lavigne, Sara Salinas, Florence Bernex, Assumpció Bosch, Vasiliki Kalatzis, Thierry Levade, Ana Maria Cuervo, Philippe Lory, Antonella Consiglio, Catarina Brito, Eric J Kremer

Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability

Cav3.2 T 型钙通道的金属/氧化还原调节的基因改变揭示了其在神经元兴奋性中的作用

期刊:Journal of Physiology-London

影响因子:2.1

doi:10.1113/JP271925

Tiphaine Voisin, Emmanuel Bourinet, Philippe Lory

神经

发表日期：2016

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A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia

CACNA1G基因的复发性突变会改变Cav3.1 T型钙通道的传导，并导致常染色体显性遗传性小脑共济失调。

期刊:American Journal of Human Genetics

影响因子:8.1

doi:10.1016/j.ajhg.2015.09.007.

Marie Coutelier ,Iulia Blesneac ,Arnaud Monteil ,Marie-Lorraine Monin ,Kunie Ando ,Emeline Mundwiller ,Alfredo Brusco ,Isabelle Le Ber ,Mathieu Anheim ,Anna Castrioto ,Charles Duyckaerts ,Alexis Brice ,Alexandra Durr ,Philippe Lory ,Giovanni Stevanin

A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis

Ca(v)3.2/syntaxin-1A信号复合物控制T型通道活性和低阈值胞吐

期刊:Journal of Biological Chemistry

影响因子:4

doi:10.1074/jbc.M111.290882

Norbert Weiss, Shahid Hameed, José M Fernández-Fernández, Katell Fablet, Maria Karmazinova, Cathy Poillot, Juliane Proft, Lina Chen, Isabelle Bidaud, Arnaud Monteil, Sylvaine Huc-Brandt, Lubica Lacinova, Philippe Lory, Gerald W Zamponi, Michel De Waard

信号转导

发表日期：2012

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T-type calcium channel inhibition underlies the analgesic effects of the endogenous lipoamino acids

型钙通道抑制是内源性脂氨基酸镇痛作用的基础

期刊:Journal of Neuroscience

影响因子:4.4

doi:10.1523/JNEUROSCI.2919-09.2009

Guillaume Barbara, Abdelkrim Alloui, Joël Nargeot, Philippe Lory, Alain Eschalier, Emmanuel Bourinet, Jean Chemin

发表日期：2009

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Structural basis for human Cav3.2 inhibition by selective antagonists

选择性拮抗剂抑制人类 Cav3.2 的结构基础

The sodium leak channel NALCN regulates cell excitability of pituitary endocrine cells

钠漏通道NALCN调节垂体内分泌细胞的细胞兴奋性

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

钠离子背景电导控制着小鼠肾上腺嗜铬细胞在原位的放电模式。

A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type Ca2+ channels

一种新的磷酸调节机制有助于 T 型 Ca2+ 通道的钙依赖性调节

Functional expression of CLIFAHDD and IHPRF pathogenic variants of the NALCN channel in neuronal cells reveals both gain- and loss-of-function properties

神经元细胞中 NALCN 通道 CLIFAHDD 和 IHPRF 致病变异的功能性表达揭示了功能获得和功能丧失的特性

Lysosomal and network alterations in human mucopolysaccharidosis type VII iPSC-derived neurons

人类粘多糖贮积症 VII 型 iPSC 衍生神经元中的溶酶体和网络改变

Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability

Cav3.2 T 型钙通道的金属/氧化还原调节的基因改变揭示了其在神经元兴奋性中的作用

A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia

CACNA1G基因的复发性突变会改变Cav3.1 T型钙通道的传导，并导致常染色体显性遗传性小脑共济失调。

A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis

Ca(v)3.2/syntaxin-1A信号复合物控制T型通道活性和低阈值胞吐

T-type calcium channel inhibition underlies the analgesic effects of the endogenous lipoamino acids

型钙通道抑制是内源性脂氨基酸镇痛作用的基础