Jing Liu, Tie-Shan Tang, Huiping Tu, Omar Nelson, Emily Herndon, Duong P Huynh, Stefan M Pulst, Ilya Bezprozvanny. J Neurosci 2009
Times Cited: 177
Times Cited: 177
Times Cited
Times Co-cited
Similarity
Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 3.
Xi Chen, Tie-Shan Tang, Huiping Tu, Omar Nelson, Mark Pook, Robert Hammer, Nobuyuki Nukina, Ilya Bezprozvanny. J Neurosci 2008
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Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2.
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Chronic suppression of inositol 1,4,5-triphosphate receptor-mediated calcium signaling in cerebellar purkinje cells alleviates pathological phenotype in spinocerebellar ataxia 2 mice.
Adebimpe W Kasumu, Xia Liang, Polina Egorova, Daria Vorontsova, Ilya Bezprozvanny. J Neurosci 2012
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Changes in Purkinje cell firing and gene expression precede behavioral pathology in a mouse model of SCA2.
Stephen T Hansen, Pratap Meera, Thomas S Otis, Stefan M Pulst. Hum Mol Genet 2013
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Deletion at ITPR1 underlies ataxia in mice and spinocerebellar ataxia 15 in humans.
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Nuclear localization or inclusion body formation of ataxin-2 are not necessary for SCA2 pathogenesis in mouse or human.
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Deranged calcium signaling in Purkinje cells and pathogenesis in spinocerebellar ataxia 2 (SCA2) and other ataxias.
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Selective positive modulator of calcium-activated potassium channels exerts beneficial effects in a mouse model of spinocerebellar ataxia type 2.
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Missense mutations in ITPR1 cause autosomal dominant congenital nonprogressive spinocerebellar ataxia.
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In vivo analysis of cerebellar Purkinje cell activity in SCA2 transgenic mouse model.
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Antisense oligonucleotide therapy for spinocerebellar ataxia type 2.
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Cloning of the gene for spinocerebellar ataxia 2 reveals a locus with high sensitivity to expanded CAG/glutamine repeats.
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Polyglutamine expansion down-regulates specific neuronal genes before pathologic changes in SCA1.
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Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor.
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Early changes in cerebellar physiology accompany motor dysfunction in the polyglutamine disease spinocerebellar ataxia type 3.
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Huntingtin and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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Total deletion and a missense mutation of ITPR1 in Japanese SCA15 families.
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SCA1 transgenic mice: a model for neurodegeneration caused by an expanded CAG trinucleotide repeat.
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Gene profiling links SCA1 pathophysiology to glutamate signaling in Purkinje cells of transgenic mice.
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Heterozygous deletion of ITPR1, but not SUMF1, in spinocerebellar ataxia type 16.
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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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Do mutations in the murine ataxia gene TRPC3 cause cerebellar ataxia in humans?
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Ataxin-2 interacts with the DEAD/H-box RNA helicase DDX6 and interferes with P-bodies and stress granules.
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Role of inositol 1,4,5-trisphosphate receptors in pathogenesis of Huntington's disease and spinocerebellar ataxias.
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Ataxin-2 and its Drosophila homolog, ATX2, physically assemble with polyribosomes.
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Decreases in the precision of Purkinje cell pacemaking cause cerebellar dysfunction and ataxia.
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Human ataxias: a genetic dissection of inositol triphosphate receptor (ITPR1)-dependent signaling.
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Ataxin-2 regulates RGS8 translation in a new BAC-SCA2 transgenic mouse model.
Warunee Dansithong, Sharan Paul, Karla P Figueroa, Marc D Rinehart, Shaina Wiest, Lance T Pflieger, Daniel R Scoles, Stefan M Pulst. PLoS Genet 2015
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Generation and characterization of Sca2 (ataxin-2) knockout mice.
Tim-Rasmus Kiehl, Alex Nechiporuk, Karla P Figueroa, Mark T Keating, Duong P Huynh, Stefan-M Pulst. Biochem Biophys Res Commun 2006
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Insulin receptor and lipid metabolism pathology in ataxin-2 knock-out mice.
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RORalpha-mediated Purkinje cell development determines disease severity in adult SCA1 mice.
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Mutant PKCγ in spinocerebellar ataxia type 14 disrupts synapse elimination and long-term depression in Purkinje cells in vivo.
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A point mutation in TRPC3 causes abnormal Purkinje cell development and cerebellar ataxia in moonwalker mice.
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Aminopyridines correct early dysfunction and delay neurodegeneration in a mouse model of spinocerebellar ataxia type 1.
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Inositol trisphosphate receptor Ca2+ release channels.
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Neuronal Atrophy Early in Degenerative Ataxia Is a Compensatory Mechanism to Regulate Membrane Excitability.
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James M Dell'Orco, Aaron H Wasserman, Ravi Chopra, Melissa A C Ingram, Yuan-Shih Hu, Vikrant Singh, Heike Wulff, Puneet Opal, Harry T Orr, Vikram G Shakkottai. J Neurosci 2015
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Cellular and circuit mechanisms underlying spinocerebellar ataxias.
Pratap Meera, Stefan M Pulst, Thomas S Otis. J Physiol 2016
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Ataxin-2 associates with the endocytosis complex and affects EGF receptor trafficking.
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Autosomal-recessive congenital cerebellar ataxia is caused by mutations in metabotropic glutamate receptor 1.
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KCa channels as therapeutic targets in episodic ataxia type-2.
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Carbonic anhydrase-related protein is a novel binding protein for inositol 1,4,5-trisphosphate receptor type 1.
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Autosomal dominant cerebellar ataxias: clinical features, genetics, and pathogenesis.
Ludger Schöls, Peter Bauer, Thorsten Schmidt, Thorsten Schulte, Olaf Riess. Lancet Neurol 2004
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Ataxin-2 associates with rough endoplasmic reticulum.
Simone van de Loo, Florian Eich, David Nonis, Georg Auburger, Joachim Nowock. Exp Neurol 2009
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Mutant ataxin-3 with an abnormally expanded polyglutamine chain disrupts dendritic development and metabotropic glutamate receptor signaling in mouse cerebellar Purkinje cells.
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TRPC3 channels are required for synaptic transmission and motor coordination.
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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.