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Times Cited: 131
Times Cited: 131
Times Cited
Times Co-cited
Similarity
Absence epilepsy in tottering mutant mice is associated with calcium channel defects.
C F Fletcher, C M Lutz, T N O'Sullivan, J D Shaughnessy, R Hawkes, W N Frankel, N G Copeland, N A Jenkins. Cell 1996
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Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNL1A4.
R A Ophoff, G M Terwindt, M N Vergouwe, R van Eijk, P J Oefner, S M Hoffman, J E Lamerdin, H W Mohrenweiser, D E Bulman, M Ferrari,[...]. Cell 1996
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Ablation of P/Q-type Ca(2+) channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the alpha(1A)-subunit.
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Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha 1A-voltage-dependent calcium channel.
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Rocker is a new variant of the voltage-dependent calcium channel gene Cacna1a.
T A Zwingman, P E Neumann, J L Noebels, K Herrup. J Neurosci 2001
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[The observation of rolling mouse Nagoya (rol), a new neurological mutant, and its maintenance (author's transl)].
S Oda. Jikken Dobutsu 1973
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Single tottering mutations responsible for the neuropathic phenotype of the P-type calcium channel.
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Altered calcium channel currents in Purkinje cells of the neurological mutant mouse leaner.
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Immunochemical identification and subcellular distribution of the alpha 1A subunits of brain calcium channels.
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Dystonia and cerebellar atrophy in Cacna1a null mice lacking P/Q calcium channel activity.
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Human epilepsy associated with dysfunction of the brain P/Q-type calcium channel.
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A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression.
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Whole-cell and single-channel analysis of P-type calcium currents in cerebellar Purkinje cells of leaner mutant mice.
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Bidirectional alterations in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice.
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Dysfunction of the brain calcium channel CaV2.1 in absence epilepsy and episodic ataxia.
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Daniela Pietrobon. Curr Opin Neurobiol 2005
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Primary structure and functional expression from complementary DNA of a brain calcium channel.
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Cerebellar cell degeneration in the leaner mutant mouse.
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Familial hemiplegic migraine mutations increase Ca(2+) influx through single human CaV2.1 channels and decrease maximal CaV2.1 current density in neurons.
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Functional consequences of mutations in the human alpha1A calcium channel subunit linked to familial hemiplegic migraine.
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An ultrastructural study of granule cell/Purkinje cell synapses in tottering (tg/tg), leaner (tg(la)/tg(la)) and compound heterozygous tottering/leaner (tg/tg(la)) mice.
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Mutations in the Cacnl1a4 calcium channel gene are associated with seizures, cerebellar degeneration, and ataxia in tottering and leaner mutant mice.
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Decreases in the precision of Purkinje cell pacemaking cause cerebellar dysfunction and ataxia.
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The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel.
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Calcium control of transmitter release at a cerebellar synapse.
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Altered calcium homeostasis in cerebellar Purkinje cells of leaner mutant mice.
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Tottering--a neuromusclar mutation in the mouse. And its linkage with oligosyndacylism.
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Mutation of the Ca2+ channel beta subunit gene Cchb4 is associated with ataxia and seizures in the lethargic (lh) mouse.
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Severely impaired neuromuscular synaptic transmission causes muscle weakness in the Cacna1a-mutant mouse rolling Nagoya.
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Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine.
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Excitatory but not inhibitory synaptic transmission is reduced in lethargic (Cacnb4(lh)) and tottering (Cacna1atg) mouse thalami.
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Complete loss of P/Q calcium channel activity caused by a CACNA1A missense mutation carried by patients with episodic ataxia type 2.
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Functional consequences of P/Q-type Ca2+ channel Cav2.1 missense mutations associated with episodic ataxia type 2 and progressive ataxia.
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Spatial learning deficit in aged heterozygous Cav2.1 channel mutant mice, rolling mouse Nagoya.
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Three new familial hemiplegic migraine mutants affect P/Q-type Ca(2+) channel kinetics.
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Familial hemiplegic migraine mutations change alpha1A Ca2+ channel kinetics.
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Loss-of-function EA2 mutations are associated with impaired neuromuscular transmission.
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Ducky mouse phenotype of epilepsy and ataxia is associated with mutations in the Cacna2d2 gene and decreased calcium channel current in cerebellar Purkinje cells.
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Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking alpha(1G) T-type Ca(2+) channels.
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Functional implications of a novel EA2 mutation in the P/Q-type calcium channel.
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Increased noise level of purkinje cell activities minimizes impact of their modulation during sensorimotor control.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.