Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases - Wikidata - wikimedia - TriplyDB

Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases

Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases

http://www.wikidata.org/entity/Q34626465

about

Mitochondrial biogenesis and dynamics in the developing and diseased heart Targeting the Pim kinases in multiple myeloma Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue.Maintaining ancient organelles: mitochondrial biogenesis and maturation.Functional Effect of Pim1 Depends upon Intracellular Localization in Human Cardiac Progenitor Cells.Pim1 kinase promotes angiogenesis through phosphorylation of endothelial nitric oxide synthase at Ser-633.Cardiac-Specific Deletion of the Pdha1 Gene Sensitizes Heart to Toxicological Actions of Ischemic Stress.Cardioprotective actions of Notch1 against myocardial infarction via LKB1-dependent AMPK signaling pathway.Personalizing cardiac regenerative therapy: At the heart of Pim1 kinase.Insulin receptor substrate 1 is a substrate of the Pim protein kinases.mTORC1 suppresses PIM3 expression via miR-33 encoded by the SREBP loci.L-Carnitine Attenuates Cardiac Dysfunction by Ischemic Insults Through Akt Signaling Pathway.Elixir of Life: Thwarting Aging With Regenerative Reprogramming.Short telomeres - A hallmark of heritable cardiomyopathies.

P2860

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P2860

Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases

http://www.wikidata.org/entity/Q34626465

description

2014 nî lūn-bûn

@nan

2014 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հունիսին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

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2014年論文

@zh-hk

2014年論文

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2014年論文

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2014年论文

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name

Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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type

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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prefLabel

Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

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CIRCRESAHA.115.304441

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Circulation Research

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Metabolic dysfunction consiste ...... s from deletion of Pim kinases

@en

P2093

Andrea De La Torre

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

Andrew S Kraft

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

Asa B Gustafsson

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Bevan Johnson

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Brett Collins

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Daniel P Kelly

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

Dieter A Kubli

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Haruhiro Toko

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Jacqueline Emathinger

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Kaitlen Samse

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P2860

Pim kinases promote cell cycle progression by phosphorylating and down-regulating p27Kip1 at the transcriptional and posttranscriptional levels

Mice deficient for all PIM kinases display reduced body size and impaired responses to hematopoietic growth factors

Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance

Prolonged AMPK Activation Increases the Expression of Fatty Acid Transporters in Cardiac Myocytes and Perfused Hearts

The hallmarks of aging

Physical and functional interactions between Pim-1 kinase and Cdc25A phosphatase. Implications for the Pim-1-mediated activation of the c-Myc signaling pathway

Activation of cardiac progenitor cells reverses the failing heart senescent phenotype and prolongs lifespan

Pim kinase-dependent inhibition of c-Myc degradation

Insulin-resistant heart exhibits a mitochondrial biogenic response driven by the peroxisome proliferator-activated receptor-alpha/PGC-1alpha gene regulatory pathway.

Telomere shortening is an in vivo marker of myocyte replication and aging.

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376-387

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scholarly article

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10.1161/CIRCRESAHA.115.304441

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3

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115

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2014-06-10T00:00:00Z

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4254755

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