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Purkinje Cell Expression of a Mutant Allele of SCA1in Transgenic Mice Leads to Disparate Effects on Motor Behaviors, Followed by a Progressive Cerebellar Dysfunction and Histological Alterations
Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurological disorder caused by the expansion of a CAG repeat encoding a polyglutamine tract. Work presented here describes theExpand
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The cerebellar leucine-rich acidic nuclear protein interacts with ataxin-1
Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder characterized by ataxia, progressive motor deterioration, and loss of cerebellar Purkinje cells. SCA1 belongsExpand
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Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation
Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder characterized by ataxia, progressive motor deterioration, and loss of cerebellar Purkinje cells. To investigate SCA1 pathogenesisExpand
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Mapmodulin/Leucine-rich Acidic Nuclear Protein Binds the Light Chain of Microtubule-associated Protein 1B and Modulates Neuritogenesis*
We had previously described the leucine-rich acidic nuclear protein (LANP) as a candidate mediator of toxicity in the polyglutamine disease, spinocerebellar ataxia type 1 (SCA1). This was based onExpand
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Anp32e/Cpd1 regulates protein phosphatase 2A activity at synapses during synaptogenesis
Anp32e/Cpd1, a member of the acidic nuclear phosphoprotein (Anp)32 family, is characterized by the presence of an amino terminal domain containing four leucine‐rich repeats and a carboxyl‐terminalExpand
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Correction: The cerebellar leucine-rich acidic nuclear protein interacts with ataxin-1
This corrects the article DOI: 10.1038/40159
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Thecerebellar leucine-rich acidic nuclear protein interactswithataxin-1
8 Note added in proof : Similar conclusions were reached by Lin et al. 29 studying the association of APL fusion proteins and SMRT. Methods Mutants, constructs and cell lines. PML–RAR␣ and PLZF–RAR␣Expand