Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice (Q28131756)

11

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author name string

Taichi Hara

1

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Kenji Nakamura

2

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Makoto Matsui

3

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Akitsugu Yamamoto

4

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Yohko Nakahara

5

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Rika Suzuki-Migishima

6

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Minesuke Yokoyama

7

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Kenji Mishima

8

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Ichiro Saito

Autophagy: in sickness and in health

9

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language of work or name

English

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publication date

15 June 2006

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published in

Nature

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volume

441

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page(s)

885-9

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issue

7095

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cites work

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Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy

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Emerging role for autophagy in the removal of aggresomes in Schwann cells.

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Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease

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Increased susceptibility of cytoplasmic over nuclear polyglutamine aggregates to autophagic degradation

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Autophagosome formation in mammalian cells

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The role of autophagy during the early neonatal starvation period

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Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice

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Bypass of lethality with mosaic mice generated by Cre– loxP -mediated recombination

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Dissection of autophagosome formation using Apg5-deficient mouse embryonic stem cells

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LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

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Progressive neuronopathy in transgenic mice expressing the human neurofilament heavy gene: a mouse model of amyotrophic lateral sclerosis

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Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

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Axonal degeneration of ascending sensory neurons in gracile axonal dystrophy mutant mouse

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Axonal abnormalities in cerebellar Purkinje cells of the 'hyperspiny Purkinje cell' mutant mouse.

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Synapse-independent and synapse-dependent apoptosis of cerebellar granule cells in postnatal rabbits occur at two subsequent but partly overlapping developmental stages

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A transgenic mouse line that retains Cre recombinase activity in mature oocytes irrespective of the cre transgene transmission.

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Inducible gene targeting in mice

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Aggresomes, inclusion bodies and protein aggregation

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Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions.

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Aggresomes protect cells by enhancing the degradation of toxic polyglutamine-containing protein

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Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

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Aggresomes formed by alpha-synuclein and synphilin-1 are cytoprotective

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p62/SQSTM1 forms protein aggregates degraded by autophagy and has a protective effect on huntingtin-induced cell death

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Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity.

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Identifiers

DOI

10.1038/NATURE04724

1 reference

Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

570971

1042871765

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570971

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference