Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy. - Wikidata - awgldk - TriplyDB

Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy.

Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy.

http://www.wikidata.org/entity/Q35126646

about

Cardiac regulation by phosphoinositide 3-kinases and PTEN Protein kinase cascades in the regulation of cardiac hypertrophy Molecular basis of physiological heart growth: fundamental concepts and new players 17ß-Estradiol regulates mTORC2 sensitivity to rapamycin in adaptive cardiac remodeling Phosphorylated Ribosomal Protein S6 Is Required for Akt-Driven Hyperplasia and Malignant Transformation, but Not for Hypertrophy, Aneuploidy and Hyperfunction of Pancreatic β-Cells Insulin Signaling and Heart Failure.Partial restoration of cardiac function with ΔPDZ nNOS in aged mdx model of Duchenne cardiomyopathy.Akt1 in the cardiovascular system: friend or foe?MTORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice.Class IA phosphoinositide 3-kinase regulates heart size and physiological cardiac hypertrophy.Folliculin (Flcn) inactivation leads to murine cardiac hypertrophy through mTORC1 deregulation Rheb (Ras homologue enriched in brain)-dependent mammalian target of rapamycin complex 1 (mTORC1) activation becomes indispensable for cardiac hypertrophic growth after early postnatal period.Myocardial loss of IRS1 and IRS2 causes heart failure and is controlled by p38α MAPK during insulin resistance.mTOR attenuates the inflammatory response in cardiomyocytes and prevents cardiac dysfunction in pathological hypertrophy.Smooth muscle protein-22-mediated deletion of Tsc1 results in cardiac hypertrophy that is mTORC1-mediated and reversed by rapamycin The role of TGFβ1 and LRG1 in cardiac remodelling and heart failure.Cardiac aging: from molecular mechanisms to significance in human health and disease mTOR signaling in mice with dysfunctional cardiac ryanodine receptor ion channel.p70 ribosomal S6 kinase regulates subpleural fibrosis following transforming growth factor-α expression in the lung The mTOR pathway in the control of protein synthesis.Cardiac restricted overexpression of kinase-dead mammalian target of rapamycin (mTOR) mutant impairs the mTOR-mediated signaling and cardiac function.Ecto-5'-nucleotidase deficiency exacerbates pressure-overload-induced left ventricular hypertrophy and dysfunction.Insulin signaling pathways and cardiac growth.Myocardial AKT: the omnipresent nexus.Akt2 regulates cardiac metabolism and cardiomyocyte survival.Mammalian target of rapamycin signaling in cardiac physiology and disease.mTORC1 signaling: what we still don't know.Drosophila models of cardiac disease.Early origins of heart disease: low birth weight and the role of the insulin-like growth factor system in cardiac hypertrophy.Characterization and regulation of mechanical loading-induced compensatory muscle hypertrophy.Fuel availability and fate in cardiac metabolism: A tale of two substrates.Cardiac mTOR complex 2 preserves ventricular function in pressure-overload hypertrophy.p70 Ribosomal S6 kinase is required for airway smooth muscle cell size enlargement but not increased contractile protein expression.Transforming growth factor-beta induces airway smooth muscle hypertrophy.ZFP260 is an inducer of cardiac hypertrophy and a nuclear mediator of endothelin-1 signaling.S6 kinase 1 knockout inhibits uninephrectomy- or diabetes-induced renal hypertrophy.Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.The death effector domain-containing DEDD supports S6K1 activity via preventing Cdk1-dependent inhibitory phosphorylation.Unique and Redundant Functions of p70 Ribosomal S6 Kinase Isoforms Regulate Mesenchymal Cell Proliferation and Migration in Pulmonary Fibrosis.Selective activation of PI3Kalpha/Akt/GSK-3beta signalling and cardiac compensatory hypertrophy during recovery from heart failure.

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P2860

Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy.

http://www.wikidata.org/entity/Q35126646

description

2004 nî lūn-bûn

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2004 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2004 թվականի հուլիսին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年論文

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2004年论文

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name

Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

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Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

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type

label

Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

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Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

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prefLabel

Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

@ast

Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

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P356

MCB.24.14.6231-6240.2004

P1433

Molecular and Cellular Biology

P1476

Deletion of ribosomal S6 kinas ...... e-induced cardiac hypertrophy.

@en

P2093

Adam L Dorfman

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

George Thomas

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

John Blenis

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

Julie R McMullen

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

Kathleen A Martin

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Li Zhang

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Mario Pende

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Megan C Sherwood

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Oleg Tarnavski

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Sarah Longnus

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P2860

S6K1(-/-)/S6K2(-/-) mice exhibit perinatal lethality and rapamycin-sensitive 5'-terminal oligopyrimidine mRNA translation and reveal a mitogen-activated protein kinase-dependent S6 kinase pathway

Regulation of ribosomal S6 kinase 2 by effectors of the phosphoinositide 3-kinase pathway

Ribosomal S6 kinase 2 inhibition by a potent C-terminal repressor domain is relieved by mitogen-activated protein-extracellular signal-regulated kinase kinase-regulated phosphorylation

Characterization of S6K2, a novel kinase homologous to S6K1

Rapamycin-FKBP specifically blocks growth-dependent activation of and signaling by the 70 kd S6 protein kinases

Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload

Specificity and mechanism of action of some commonly used protein kinase inhibitors

Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study

Mammalian cell size is controlled by mTOR and its downstream targets S6K1 and 4EBP1/eIF4E

Amino acid-induced translation of TOP mRNAs is fully dependent on phosphatidylinositol 3-kinase-mediated signaling, is partially inhibited by rapamycin, and is independent of S6K1 and rpS6 phosphorylation

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6231-6240

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10.1128/MCB.24.14.6231-6240.2004

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