RORalpha-mediated Purkinje cell development determines disease severity in adult SCA1 mice (Q24316105)

GOA release 2020-03-11

Ataxin 1

1 reference

K(lysine) acetyltransferase 5

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

Harry T Orr

12

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Huda Zoghbi

object named as

Huda Y Zoghbi

9

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J. Michael Andresen

11

object named as

J Michael Andresen

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author name string

Heliane G Serra

1

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Lisa Duvick

2

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Tao Zu

3

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Kerri Carlson

4

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Sam Stevens

5

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Nathan Jorgensen

6

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Alana Lysholm

7

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Eric Burright

8

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H Brent Clark

Electron microscopic analysis of postnatal histogenesis in the cerebellar cortex of staggerer mutant mice

10

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language of work or name

English

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publication date

17 November 2006

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published in

Cell

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volume

127

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issue

4

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page(s)

697-708

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cites work

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SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat

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Early dendritic development of Purkinje cells in the rat cerebellum. A light and electron microscopic study using axonal tracing in 'in vitro' slices

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The AXH domain of Ataxin-1 mediates neurodegeneration through its interaction with Gfi-1/Senseless proteins

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The AXH module: an independently folded domain common to ataxin-1 and HBP1

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Ataxin-1 nuclear localization and aggregation: role in polyglutamine-induced disease in SCA1 transgenic mice.

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Interaction of Akt-phosphorylated ataxin-1 with 14-3-3 mediates neurodegeneration in spinocerebellar ataxia type 1.

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Progressive atrophy of cerebellar Purkinje cell dendrites during aging of the heterozygous staggerer mouse (Rora(+/sg)).

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The cells and molecules that make a cerebellum.

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Prominent expression of nuclear hormone receptor ROR alpha in Purkinje cells from early development.

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Mutation of the E6-AP ubiquitin ligase reduces nuclear inclusion frequency while accelerating polyglutamine-induced pathology in SCA1 mice.

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Interaction between mutant ataxin-1 and PQBP-1 affects transcription and cell death

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A long CAG repeat in the mouse Sca1 locus replicates SCA1 features and reveals the impact of protein solubility on selective neurodegeneration.

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Serine 776 of ataxin-1 is critical for polyglutamine-induced disease in SCA1 transgenic mice

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RORalpha coordinates reciprocal signaling in cerebellar development through sonic hedgehog and calcium-dependent pathways

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Orphan nuclear receptor ROR alpha-deficient mice display the cerebellar defects of staggerer.

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Postnatal cerebellar cells from staggerer mutant mice express embryonic cell surface characteristic

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Identification of genes that modify ataxin-1-induced neurodegeneration.

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Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor.

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Disruption of the nuclear hormone receptor RORalpha in staggerer mice

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Ataxin-1 with an expanded glutamine tract alters nuclear matrix-associated structures

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Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1.

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Polyglutamine expansion down-regulates specific neuronal genes before pathologic changes in SCA1.

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Expression analysis of the ataxin-1 protein in tissues from normal and spinocerebellar ataxia type 1 individuals

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Spectrin mutations cause spinocerebellar ataxia type 5.

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Controlling nuclear receptors: the circular logic of cofactor cycles

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Boat, an AXH domain protein, suppresses the cytotoxicity of mutant ataxin-1.

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Ataxin 1, a SCA1 neurodegenerative disorder protein, is functionally linked to the silencing mediator of retinoid and thyroid hormone receptors

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Ataxia and altered dendritic calcium signaling in mice carrying a targeted null mutation of the calbindin D28k gene

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staggerer phenotype in retinoid-related orphan receptor alpha-deficient mice.

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Tip60 is a nuclear hormone receptor coactivator

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The co-repressor hairless protects RORalpha orphan nuclear receptor from proteasome-mediated degradation

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The structure of the AXH domain of spinocerebellar ataxin-1

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The spinocerebellar ataxia type 1 protein, ataxin-1, has RNA-binding activity that is inversely affected by the length of its polyglutamine tract

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Over-expression of inducible HSP70 chaperone suppresses neuropathology and improves motor function in SCA1 mice

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Cloning and developmental expression analysis of the murine homolog of the spinocerebellar ataxia type 1 gene (Sca1).

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Identification of a self-association region within the SCA1 gene product, ataxin-1

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Gene profiling links SCA1 pathophysiology to glutamate signaling in Purkinje cells of transgenic mice

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Spinocerebellar ataxia type 1--modeling the pathogenesis of a polyglutamine neurodegenerative disorder in transgenic mice

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Toxic proteins in neurodegenerative disease

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mGluR1 in cerebellar Purkinje cells essential for long-term depression, synapse elimination, and motor coordination

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Glutamine repeats and neurodegeneration

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Immunohistochemical characterization of the orphan nuclear receptor ROR alpha in the mouse nervous system.

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Amino acids in a region of ataxin-1 outside of the polyglutamine tract influence the course of disease in SCA1 transgenic mice.

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Purkinje cell expression of a mutant allele of SCA1 in transgenic mice leads to disparate effects on motor behaviors, followed by a progressive cerebellar dysfunction and histological alterations.

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Mice lacking ataxin-1 display learning deficits and decreased hippocampal paired-pulse facilitation

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Recovery from polyglutamine-induced neurodegeneration in conditional SCA1 transgenic mice.

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Climbing fiber activation of EAAT4 transporters and kainate receptors in cerebellar Purkinje cells

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