Modulation of the Ca2+ permeability of human endplate acetylcholine receptor-channel-Reference-Cited by-同舟云学术

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Modulation of the Ca2+ permeability of human endplate acetylcholine receptor-channel

Published:2011-04 Issue:4 Volume:49 Page:272-278
ISSN:0143-4160
Container-title:Cell Calcium
language:en
Short-container-title:Cell Calcium

Author:

Piccari Vanessa,Deflorio Cristina,Bigi Rachele,Grassi Francesca,Fucile Sergio

Funder

Sapienza Università di Roma

Association Française contre les Myopathies

Ministero della Salute

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Physiology

Reference37 articles.

1. Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit;Ohno;Proc. Natl. Acad. Sci. U.S.A.,1995

2. Congenital myasthenic syndromes: a diverse array of molecular targets;Engel;J. Neurocytol.,2003

3. Active calcium accumulation underlies severe weakness in a panel of mice with slow-channel syndrome;Gomez;J. Neurosci.,2002

4. The human adult subtype ACh receptor channel has high Ca2+ permeability and predisposes to endplate Ca2+ overloading;Fucile;J. Physiol.,2006

5. Inositol-14,5-triphosphate receptors mediate activity-induced synaptic Ca2+ signals in muscle fibers and Ca2+ overload in slow-channel syndrome;Zayas;Cell Calcium,2007

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2. “Calcium bombs” as harbingers of synaptic pathology and their mitigation by magnesium at murine neuromuscular junctions;Frontiers in Molecular Neuroscience;2022-07-26

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4. Calcium influx through muscle nAChR-channels: One route, multiple roles;Neuroscience;2020-07

5. Extracellular mild acidosis decreases the Ca2+ permeability of the human NMDA receptors;Cell Calcium;2019-06

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