d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in Drosophila. - Wikidata - awgldk - TriplyDB

d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in Drosophila.

d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in Drosophila.

http://www.wikidata.org/entity/Q30493481

about

Sestrins at the crossroad between stress and aging A Drosophila model of high sugar diet-induced cardiomyopathy Quality control systems in cardiac aging Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies High-fat-diet-induced obesity and heart dysfunction are regulated by the TOR pathway in Drosophila Altered proteome turnover and remodeling by short-term caloric restriction or rapamycin rejuvenate the aging heart.Impact papers on aging in 2009.Aging and CaMKII alter intracellular Ca2+ transients and heart rhythm in Drosophila melanogaster.Ageing in Drosophila: the role of the insulin/Igf and TOR signalling network.Drosophila, genetic screens, and cardiac function TOR and ageing: a complex pathway for a complex process.Phospholipid homeostasis regulates lipid metabolism and cardiac function through SREBP signaling in Drosophila Role of TOR signaling in aging and related biological processes in Drosophila melanogaster Drosophila as a model to study cardiac aging dFOXO-independent effects of reduced insulin-like signaling in Drosophila.Drosophila Longevity Assurance Conferred by Reduced Insulin Receptor Substrate Chico Partially Requires d4eBP.Interplay between FOXO, TOR, and Akt.Rejuvenating immunity: "anti-aging drug today" eight years later.Dietary composition regulates Drosophila mobility and cardiac physiology.Development of diet-induced insulin resistance in adult Drosophila melanogaster.Two phases of aging separated by the Smurf transition as a public path to death.Answering the ultimate question "what is the proximal cause of aging?"Hot topics in aging research: protein translation, 2009.Pygopus maintains heart function in aging Drosophila independently of canonical Wnt signaling Molecular mechanisms of heart failure: insights from Drosophila 4E-BP is a target of the GCN2-ATF4 pathway during Drosophila development and aging.Stressin' Sestrins take an aging fight.Obesity and nutrient sensing TOR pathway in flies and vertebrates: Functional conservation of genetic mechanisms.Drosophila models of cardiac disease.Genetic manipulation of cardiac ageing.The Aging Heart Gaining Insights into Diabetic Cardiomyopathy from Drosophila.Drosophila in the Heart of Understanding Cardiac Diseases: Modeling Channelopathies and Cardiomyopathies in the Fruitfly.Drosophila melanogaster as a Model for Diabetes Type 2 Progression.

P2860

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P2860

d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in Drosophila.

http://www.wikidata.org/entity/Q30493481

description

2009 nî lūn-bûn

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2009 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2009 թվականի հուլիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

d4eBP acts downstream of both ...... unctional aging in Drosophila.

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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J.1474-9726.2009.00504.X

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d4eBP acts downstream of both ...... unctional aging in Drosophila.

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P2093

Claire Davies

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Erin Fitzgerald

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Hui-Ying Lim

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Karen Ocorr

http://www.w3.org/2001/XMLSchema#string

Lisa Elmén

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Michael Hayes

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Nicole Piazza

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Robert Wessells

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Rolf Bodmer

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Samantha Morley

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P2860

Insulin-dependent stimulation of protein synthesis by phosphorylation of a regulator of 5'-cap function

Drosophila lacking microRNA miR-278 are defective in energy homeostasis

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

Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway

KCNQ potassium channel mutations cause cardiac arrhythmias in Drosophila that mimic the effects of aging.

RAFT1 phosphorylation of the translational regulators p70 S6 kinase and 4E-BP1

The Drosophila forkhead transcription factor FOXO mediates the reduction in cell number associated with reduced insulin signaling

Targeted gene expression as a means of altering cell fates and generating dominant phenotypes

Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein

Upstream and downstream of mTOR

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542-552

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10.1111/J.1474-9726.2009.00504.X

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5

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