Ion channels in genetic and acquired forms of epilepsy

Ion channels in genetic and acquired forms of epilepsy

Veure altres versions (1)

Genetic mutations causing dysfunction of both voltage- and ligand-gated ion channels make a major contribution to the cause of many different types of familial epilepsy. Key mechanisms comprise defective Na+ channels of inhibitory neurons, or GABAA receptors affecting pre- or postsynaptic GABAergic...

Descripció completa

Dades bibliogràfiques
Autors principals:	Lerche, H, Shah, M, Beck, H, Noebels, J, Johnston, D, Vincent, A
Format:	Journal article
Publicat:	2013

Ítems similars

Ion channels in genetic and acquired forms of epilepsy.
per: Lerche, H, et al.
Publicat: (2013)

Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies
per: Karen M. J. van Loo, et al.
Publicat: (2020-01-01)

Editorial: Ion-channels in epilepsy
per: Enes Akyuz, et al.
Publicat: (2023-08-01)

Molecular Genetics of Acquired Temporal Lobe Epilepsy
per: Anne-Marie Neumann, et al.
Publicat: (2024-06-01)

Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential
per: Jakob eWolfart, et al.
Publicat: (2015-06-01)

Neuronal voltage-gated ion channels are genetic modifiers of generalized epilepsy with febrile seizures plus
per: Nicole A. Hawkins, et al.
Publicat: (2011-03-01)

Idiopathic and symptomatic forms of genetic epilepsy
per: A. G. Malov
Publicat: (2022-04-01)

Voltage-gated potassium channels and genetic epilepsy
per: Yiting Zheng, et al.
Publicat: (2024-10-01)

Diurnal circadian clock gene expression is altered in models of genetic and acquired epilepsy
per: Glenn R. Yamakawa, et al.
Publicat: (2023-12-01)

Editorial: Neuroinflammation in acquired epilepsy
per: Jianxiong Jiang, et al.
Publicat: (2022-11-01)

Alternative ion channel splicing in mesial temporal lobe epilepsy and Alzheimer's disease.
per: Heinzen, E, et al.
Publicat: (2007)

Antibodies to voltage-gated potassium and calcium channels in epilepsy.
per: Majoie, H, et al.
Publicat: (2006)

Ion channel stability and hydrogen bonding molecular modelling of channels formed by synthetic alamethicin analogues
per: Breed, J, et al.
Publicat: (1997)

Genetic Variation in Calcium Channel Gene in Idiopathic Generalized Epilepsies
per: J Gordon Millichap
Publicat: (2008-01-01)

Function of acid-sensing ion channels and its influence in the development of epilepsy
per: Qing-qing CAO, et al.
Publicat: (2014-11-01)

Genetic heterogeneity in familial forms of genetic generalized epilepsy: from mono- to oligogenism
per: Maha Dahawi, et al.
Publicat: (2024-11-01)

Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence epilepsy
per: M.K. Oliva, et al.
Publicat: (2014-07-01)

Epilepsy, Acquired Aphasia with Focal Cortical Dysplasia
per: Girija A.S, et al.
Publicat: (1999-01-01)

Neurodegenerative pathways as targets for acquired epilepsy therapy development
per: Pablo M. Casillas‐Espinosa, et al.
Publicat: (2020-06-01)

Antibodies affecting ion channel function in acquired neuromyotonia, in seropositive and seronegative myasthenia gravis, and in antibody-mediated arthrogryposis multiplex congenita.
per: Vincent, A, et al.
Publicat: (1998)

Deleterious Rare Variants Reveal Risk for Loss of GABAA Receptor Function in Patients with Genetic Epilepsy and in the General Population.
per: Ciria C Hernandez, et al.
Publicat: (2016-01-01)

Subthreshold changes of voltage-dependent activation of the KV7.2 channel in neonatal epilepsy
per: Jessica Hunter, et al.
Publicat: (2006-10-01)

Genetic Analysis of Sodium Channel Genes in Pediatric Epilepsy Patients of Pakistan
per: Aqsa Ashfaq, et al.
Publicat: (2022-01-01)

Editorial: Ion channels and transporters in epilepsy: From genes and mechanisms to disease-targeted therapies
per: Hailan He, et al.
Publicat: (2022-09-01)

Regional and Subunit-Specific Downregulation of Acid-Sensing Ion Channels in the Pilocarpine Model of Epilepsy
per: Giuseppe Biagini, et al.
Publicat: (2001-02-01)

Correction: Deleterious Rare Variants Reveal Risk for Loss of GABAA Receptor Function in Patients with Genetic Epilepsy and in the General Population.
per: Ciria C Hernandez, et al.
Publicat: (2016-01-01)

Mutant SOD1 forms ion channel: Implications for ALS pathophysiology
per: Michael J. Allen, et al.
Publicat: (2012-03-01)

Magnetoencephalography Reveals a Widespread Increase in Network Connectivity in Idiopathic/Genetic Generalized Epilepsy.
per: Adham Elshahabi, et al.
Publicat: (2015-01-01)

NMR Studies of the Ion Channel-Forming Human Amyloid-β with Zinc Ion Concentrations
per: Minseon Kim, et al.
Publicat: (2021-10-01)

Multi-spectral diffusion MRI mega-analysis in genetic generalized epilepsy: Relation to outcomes
per: Barbara A.K. Kreilkamp, et al.
Publicat: (2023-01-01)

Does gender influence susceptibility and consequences of acquired epilepsies?
per: Piero Perucca, et al.
Publicat: (2014-12-01)

Autoantibodies to ion channels at the neuromuscular junction.
per: Lang, B, et al.
Publicat: (2003)

Predicting functional effects of ion channel variants using new phenotypic machine learning methods.
per: Christian Malte Boßelmann, et al.
Publicat: (2023-03-01)

Genetically engineered metal ion binding sites on the outside of a Channel's transmembrane beta-barrel.
per: Kasianowicz, J, et al.
Publicat: (1999)

Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy
per: Minyoung Shin, et al.
Publicat: (2008-10-01)

Ion channel trafficking: Control of ion channel density as a target for arrhythmias?
per: Balse, E, et al.
Publicat: (2017)

Identification of an epilepsy-linked gut microbiota signature in a pediatric rat model of acquired epilepsy
per: Antonella Riva, et al.
Publicat: (2024-05-01)

Acquiring and analyzing back-channels
per: Phan Anh Tuan
Publicat: (2015)

Metabolic correction by pyruvate halts acquired epilepsy in multiple rodent models
per: I. Popova, et al.
Publicat: (2017-10-01)

Genetics of Childhood Epilepsy
per: J Gordon Millichap
Publicat: (2000-03-01)