Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia-reperfusion-induced cell death in vivo. - Wikidata - wikimedia - TriplyDB

Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia-reperfusion-induced cell death in vivo.

Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia-reperfusion-induced cell death in vivo.

http://www.wikidata.org/entity/Q46618468

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Plasma membrane Ca2+-ATPase isoform 4 antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodents Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4-JNK pathway DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility Jun kinase delays caspase-9 activation by interaction with the apoptosome Forced expression of the cell cycle inhibitor p57Kip2 in cardiomyocytes attenuates ischemia-reperfusion injury in the mouse heart.RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways.TRPC channels are necessary mediators of pathologic cardiac hypertrophy.Post-conditioning protecting rat cardiomyocytes from apoptosis via attenuating calcium-sensing receptor-induced endo(sarco)plasmic reticulum stress.c-Jun N-terminal kinase phosphorylation of stathmin confers protection against cellular stress Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives Myocardial loss of IRS1 and IRS2 causes heart failure and is controlled by p38α MAPK during insulin resistance.Inhibition of JNK aggravates the recovery of rat hearts after global ischemia: the role of mitochondrial JNK.c-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction.Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation Update on the Pathophysiological Role of Intracellular Signaling Pathways in Atherosclerotic Plaques and Ischemic Myocardium Nemo-Like Kinase (NLK) Is a Pathological Signaling Effector in the Mouse Heart.Nitric oxide mediates cardiac protection of tissue kallikrein by reducing inflammation and ventricular remodeling after myocardial ischemia/reperfusion.The virtue of just enough stress: a molecular model.Role of xanthine oxidoreductase in cardiac nitroso-redox imbalance Inhibition of JNK mitochondrial localization and signaling is protective against ischemia/reperfusion injury in rats.Knockout of the c-Jun N-terminal Kinase 2 aggravates the development of mild chronic dextran sulfate sodium colitis independently of expression of intestinal cytokines TNFα, TGFB1, and IL-6.Ischemic preconditioning in solid organ transplantation: from experimental to clinics.Imaging of receptors for advanced glycation end products in experimental myocardial ischemia and reperfusion injury Stromal cell derived factor-1 alpha confers protection against myocardial ischemia/reperfusion injury: role of the cardiac stromal cell derived factor-1 alpha CXCR4 axis.AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia.Tumor necrosis factor-induced toxic liver injury results from JNK2-dependent activation of caspase-8 and the mitochondrial death pathway Mitogen-activated protein kinases in heart development and diseases c-Jun N-terminal kinases as potential therapeutic targets.DUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.Inducible and myocyte-specific inhibition of PKCalpha enhances cardiac contractility and protects against infarction-induced heart failure.Genetic manipulation of periostin expression in the heart does not affect myocyte content, cell cycle activity, or cardiac repair Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling.Cdc42 is an antihypertrophic molecular switch in the mouse heart.Inhibition of the activity of poly (ADP-ribose) polymerase reduces heart ischaemia/reperfusion injury via suppressing JNK-mediated AIF translocation.ASK1 regulates cardiomyocyte death but not hypertrophy in transgenic mice FoxO transcription factors promote autophagy in cardiomyocytes Cell biology of ischemia/reperfusion injury.Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury.

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P2860

Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia-reperfusion-induced cell death in vivo.

http://www.wikidata.org/entity/Q46618468

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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name

Genetic inhibition or activati ...... on-induced cell death in vivo.

@en

Genetic inhibition or activati ...... on-induced cell death in vivo.

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type

label

Genetic inhibition or activati ...... on-induced cell death in vivo.

@en

Genetic inhibition or activati ...... on-induced cell death in vivo.

@nl

prefLabel

Genetic inhibition or activati ...... on-induced cell death in vivo.

@en

Genetic inhibition or activati ...... on-induced cell death in vivo.

@nl

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P1433

Journal of Biological Chemistry

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Genetic inhibition or activati ...... on-induced cell death in vivo.

@en

P2093

Orlando Bueno

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

Qiangrong Liang

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

Raisa Klevitsky

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

Robert A Kaiser

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Timothy E Hewett

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Troy Lackey

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

Yuan Huang

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

P2860

JNK suppresses apoptosis via phosphorylation of the proapoptotic Bcl-2 family protein BAD

Convergence of MAP kinase pathways on the ternary complex factor Sap-1a.

The Bax subfamily of Bcl2-related proteins is essential for apoptotic signal transduction by c-Jun NH(2)-terminal kinase

JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis

MEKK1 suppresses oxidative stress-induced apoptosis of embryonic stem cell-derived cardiac myocytes

p21-activated kinase 1 phosphorylates the death agonist bad and protects cells from apoptosis

Signal transduction by the JNK group of MAP kinases

The PIM-2 kinase phosphorylates BAD on serine 112 and reverses BAD-induced cell death

Mitochondrial PKCepsilon and MAPK form signaling modules in the murine heart: enhanced mitochondrial PKCepsilon-MAPK interactions and differential MAPK activation in PKCepsilon-induced cardioprotection

Role of MEKK1 in cell survival and activation of JNK and ERK pathways defined by targeted gene disruption

P304

32602-32608

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scholarly article

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10.1074/JBC.M500684200

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38

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280

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Jeffery D. Molkentin

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2005-07-25T00:00:00Z

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16043490

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