Genome-wide RNAi screen and in vivo protein aggregation reporters identify degradation of damaged proteins as an essential hypertonic stress response (Q37016726)

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scientific article published on October 2008

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English	Genome-wide RNAi screen and in vivo protein aggregation reporters identify degradation of damaged proteins as an essential hypertonic stress response	scientific article published on October 2008

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scholarly article

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

Genome-wide RNAi screen and in vivo protein aggregation reporters identify degradation of damaged proteins as an essential hypertonic stress response (English)

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

protein aggregation

1 reference

based on heuristic

inferred from title

author name string

Keith P Choe

1

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

Kevin Strange

2

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

publication date

1 October 2008

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Europe PubMed Central

PMC publication ID

17 August 2017

American Journal of Physiology - Cell Physiology

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Europe PubMed Central

PMC publication ID

17 August 2017

295

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

6

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

C1488-98

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

describes a project that uses

1 reference

Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC2603564/fullTextXML

based on heuristic

inferred from PubMed Central ID database lookup

Guiding protein aggregation with macromolecular crowding

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2603564

29 September 2017

Macromolecular crowding and confinement: biochemical, biophysical, and potential physiological consequences

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2603564

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Functional multivesicular bodies are required for autophagic clearance of protein aggregates associated with neurodegenerative disease

1 reference

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Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

1 reference

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Molecular and genetic characterization of osmosensing and signal transduction in the nematode Caenorhabditis elegans

1 reference

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Cellular response to hyperosmotic stresses

1 reference

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Protein stress and stress proteins: implications in aging and disease

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Hyperosmotic stress response: comparison with other cellular stresses

1 reference

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The fly as a model for neurodegenerative diseases: is it worth the jump?

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Amyloidosis-associated kidney disease

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Genome-wide RNAi screening identifies protein damage as a regulator of osmoprotective gene expression

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Potential compensatory responses through autophagic/lysosomal pathways in neurodegenerative diseases

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ALS phenotypes with mutations in CHMP2B (charged multivesicular body protein 2B)

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Protein aggregation in crowded environments.

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Oxidative stress promotes mutant huntingtin aggregation and mutant huntingtin-dependent cell death by mimicking proteasomal malfunction.

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Cell survival in the hostile environment of the renal medulla

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Toward improving Caenorhabditis elegans phenome mapping with an ORFeome-based RNAi library

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Decreased proteolysis caused by protein aggregates, inclusion bodies, plaques, lipofuscin, ceroid, and 'aggresomes' during oxidative stress, aging, and disease.

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Protein aggregation and neurodegenerative disease

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Hyperosmolality triggers oxidative damage in kidney cells

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High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNA

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Genome-wide RNA interference screen identifies previously undescribed regulators of polyglutamine aggregation

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A conserved siRNA-degrading RNase negatively regulates RNA interference in C. elegans.

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Protein aggregation and aggregate toxicity: new insights into protein folding, misfolding diseases and biological evolution

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Inhibition of proteasomal activity causes inclusion formation in neuronal and non-neuronal cells overexpressing Parkin

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SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response

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Protein misfolding, aggregation, and degradation in disease

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Systematic functional analysis of the Caenorhabditis elegans genome using RNAi

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Chemical chaperones reduce aggregate formation and cell death caused by the truncated Machado-Joseph disease gene product with an expanded polyglutamine stretch

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The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans

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How crowded is the cytoplasm?

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Commentary. Lysosomotropic agents

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Effects of osmolarity, ions and compatible osmolytes on cell-free protein synthesis

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Evolutionarily conserved WNK and Ste20 kinases are essential for acute volume recovery and survival after hypertonic shrinkage in Caenorhabditis elegans

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Polyglutamine protein aggregates are dynamic

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Identifiers

10.1152/AJPCELL.00450.2008

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

PMC publication ID

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PMC publication ID

17 August 2017

ResearchGate publication ID

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