Autophagy is involved in the elimination of intracellular inclusions, Mallory-Denk bodies, in hepatocytes (Q43117841)

14 November 2017

Autophagy is involved in the elimination of intracellular inclusions, Mallory-Denk bodies, in hepatocytes (English)

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14 November 2017

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Masaru Harada

1

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PubMed ID

20340001

14 November 2017

language of work or name

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26 March 2010

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Medical Molecular Morphology

14 November 2017

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14 November 2017

43

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14 November 2017

1

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14 November 2017

13-18

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https://scigraph.springernature.com/pub.10.1007/s00795-009-0476-5

14 November 2017

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cites work

Cytokeratin 8 protects from hepatotoxicity, and its ratio to cytokeratin 18 determines the ability of hepatocytes to form Mallory bodies

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Methods for monitoring autophagy

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Lithium induces autophagy by inhibiting inositol monophosphatase

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Intracellular inclusions containing mutant alpha1-antitrypsin Z are propagated in the absence of autophagic activity

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Keratin 18 overexpression but not phosphorylation or filament organization blocks mouse Mallory body formation

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Trehalose, a novel mTOR-independent autophagy enhancer, accelerates the clearance of mutant huntingtin and alpha-synuclein.

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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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HDAC6 and microtubules are required for autophagic degradation of aggregated huntingtin

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p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagy

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Involvement of macroautophagy in the dissolution of neuronal inclusions.

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Mallory bodies revisited

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Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice

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Autophagy modulates keratin-containing inclusion formation and apoptosis in cell culture in a context-dependent fashion.

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12 December 2020

The keratin cytoskeleton in liver diseases

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Modification of proteins by ubiquitin and ubiquitin-like proteins

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Congenital myopathies at their molecular dawning

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Immunohistochemical profiles of Mallory body by a panel of anti-cytokeratin antibodies

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Proteasome inhibition induces inclusion bodies associated with intermediate filaments and fragmentation of the Golgi apparatus.

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Keratins let liver live: Mutations predispose to liver disease and crosslinking generates Mallory-Denk bodies.

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Cytoskeletal alterations leading to Mallory body formation in livers of mice fed 3,5-diethoxycarbonyl-1,4-dihydrocollidine

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Lessons from keratin 18 knockout mice: formation of novel keratin filaments, secondary loss of keratin 7 and accumulation of liver-specific keratin 8-positive aggregates

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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

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Autophagy in the Pathogenesis of Disease

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12 December 2020

From Mallory to Mallory-Denk bodies: what, how and why?

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Keratin 8 overexpression promotes mouse Mallory body formation

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Autophagy: in sickness and in health

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Linking of autophagy to ubiquitin-proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability

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Loss of autophagy in the central nervous system causes neurodegeneration in mice

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12 December 2020

Autophagy activation by rapamycin eliminates mouse Mallory-Denk bodies and blocks their proteasome inhibitor-mediated formation.

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12 December 2020

Studying simple epithelial keratins in cells and tissues.

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12 December 2020

10.1007/S00795-009-0476-5

Identifiers

DOI

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14 November 2017

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PubMed ID

20340001