Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells. - sprookjes - yvandenbroek - TriplyDB

Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells.

Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells.

http://www.wikidata.org/entity/Q34196369

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Targeting protein prenylation in progeria mTOR is a key modulator of ageing and age-related disease Inhibition of the Mechanistic Target of Rapamycin (mTOR)-Rapamycin and Beyond Molecular insights into the premature aging disease progeria When lamins go bad: nuclear structure and disease Mouse models of laminopathies Nuclear lamins and oxidative stress in cell proliferation and longevity Degradation-mediated protein quality control at the inner nuclear membrane Potential therapeutic effects of the MTOR inhibitors for preventing ageing and progeria-related disorders Recent advances in understanding the role of lamins in health and disease Better Living through Chemistry: Caloric Restriction (CR) and CR Mimetics Alter Genome Function to Promote Increased Health and Lifespan Sex- and tissue-specific changes in mTOR signaling with age in C57BL/6J mice The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging Rapalogs and mTOR inhibitors as anti-aging therapeutics Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype Rapamycin induces pluripotent genes associated with avoidance of replicative senescence Lysosome-mediated processing of chromatin in senescence.Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism Prelamin A accumulation and stress conditions induce impaired Oct-1 activity and autophagy in prematurely aged human mesenchymal stem cell HP1α mediates defective heterochromatin repair and accelerates senescence in Zmpste24-deficient cells.Sustained activation of DNA damage response in irradiated apoptosis-resistant cells induces reversible senescence associated with mTOR downregulation and expression of stem cell markers Mechanisms controlling the smooth muscle cell death in progeria via down-regulation of poly(ADP-ribose) polymerase 1.DNA damage and lamins Metformin decreases progerin expression and alleviates pathological defects of Hutchinson-Gilford progeria syndrome cells.Inducing autophagy by rapamycin before, but not after, the formation of plaques and tangles ameliorates cognitive deficits.DNA-damage accumulation and replicative arrest in Hutchinson-Gilford progeria syndrome A novel library screen identifies immunosuppressors that promote osteoblast differentiation.Cell autonomous and systemic factors in progeria development.Progeria: translational insights from cell biology.Can Hutchinson-Gilford progeria syndrome be cured in the future?DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Rapamycin treatment of Mandibuloacral dysplasia cells rescues localization of chromatin-associated proteins and cell cycle dynamics Senescence and apoptosis: dueling or complementary cell fates?From cellular characteristics to disease diagnosis: uncovering phenotypes with supercells.Sulforaphane enhances progerin clearance in Hutchinson-Gilford progeria fibroblasts.TOR in the immune system.Perspectives of Targeting mTORC1-S6K1 in Cardiovascular Aging NCI's provocative questions on cancer: some answers to ignite discussion.Automated image analysis of nuclear shape: what can we learn from a prematurely aged cell?

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Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells.

http://www.wikidata.org/entity/Q34196369

description

2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Science Translational Medicine

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Rapamycin reverses cellular ph ...... lford progeria syndrome cells.

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Cecilia D Blair

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Dimitri Krainc

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John J Graziotto

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Joseph R Mazzulli

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P2860

The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin

A new protein conjugation system in human. The counterpart of the yeast Apg12p conjugation system essential for autophagy

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

The selective macroautophagic degradation of aggregated proteins requires the PI3P-binding protein Alfy

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

Extension of chronological life span in yeast by decreased TOR pathway signaling

Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

Phenotype and course of Hutchinson-Gilford progeria syndrome

Reduced TOR signaling extends chronological life span via increased respiration and upregulation of mitochondrial gene expression

A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model

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