Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice. - Wikidata - awgldk - TriplyDB

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

http://www.wikidata.org/entity/Q44438374

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BRCA1 is an essential regulator of heart function and survival following myocardial infarction Good and bad sides of TGFβ-signaling in myocardial infarction BAX unleashed: the biochemical transformation of an inactive cytosolic monomer into a toxic mitochondrial pore Mitochondria and mitophagy: the yin and yang of cell death control Apoptosis: a review of programmed cell death Regulation of signal transduction by reactive oxygen species in the cardiovascular system Bax regulates primary necrosis through mitochondrial dynamics Popeye domain containing 1 (Popdc1/Bves) is a caveolae-associated protein involved in ischemia tolerance Apoptosis repressor with a CARD domain (ARC) restrains Bax-mediated pathogenesis in dystrophic skeletal muscle Heme oxygenase-1 induction improves cardiac function following myocardial ischemia by reducing oxidative stress Leptin attenuates hypoxia/reoxygenation-induced activation of the intrinsic pathway of apoptosis in rat H9c2 cells.mTORC2 phosphorylation of Akt1: a possible mechanism for hydrogen sulfide-induced cardioprotection.Role of autophagy and apoptosis in wound tissue of deep second-degree burn in rats.Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases TanshinoneIIA and cryptotanshinone protect against hypoxia-induced mitochondrial apoptosis in H9c2 cells.FoxO transcription factors promote cardiomyocyte survival upon induction of oxidative stress.Role of the mitochondrion in programmed necrosis The mitochondrial dynamism-mitophagy-cell death interactome: multiple roles performed by members of a mitochondrial molecular ensemble.Rapamycin reduces burn wound progression by enhancing autophagy in deep second-degree burn in rats.Prenatal cocaine exposure increases apoptosis of neonatal rat heart and heart susceptibility to ischemia-reperfusion injury in 1-month-old rat.Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion Adiponectin protects rat myocardium against chronic intermittent hypoxia-induced injury via inhibition of endoplasmic reticulum stress.bFGF attenuates endoplasmic reticulum stress and mitochondrial injury on myocardial ischaemia/reperfusion via activation of PI3K/Akt/ERK1/2 pathway.Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.Cardiomyocyte death: mechanisms and translational implications Statin and resveratrol in combination induces cardioprotection against myocardial infarction in hypercholesterolemic rat Long-Lived αMUPA Mice Show Attenuation of Cardiac Aging and Leptin-Dependent Cardioprotection.BRCA2 protein deficiency exaggerates doxorubicin-induced cardiomyocyte apoptosis and cardiac failure FAK regulates cardiomyocyte survival following ischemia/reperfusion.Effects of buyang huanwu decoction on ventricular remodeling and differential protein profile in a rat model of myocardial infarction.Bcl-2 family members and apoptosis, taken to heart.Functional hepatocyte culture and its application to cell therapies.Myocardial AKT: the omnipresent nexus.Decreased expression level of apoptosis-related genes and/or proteins in skeletal muscles, but not in hearts, of growth hormone receptor knockout mice Decreased levels of proapoptotic factors and increased key regulators of mitochondrial biogenesis constitute new potential beneficial features of long-lived growth hormone receptor gene-disrupted mice.Cyclin-dependent kinase 2 signaling regulates myocardial ischemia/reperfusion injury.Programmed cell death in cardiac myocytes: strategies to maximize post-ischemic salvage.The mitochondrial permeability transition pore and ischemia-reperfusion injury Nuclear and mitochondrial signalling Akts in cardiomyocytes

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Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

http://www.wikidata.org/entity/Q44438374

description

2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年学术文章

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2003年學術文章

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2003年學術文章

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name

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@en

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@nl

type

label

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@en

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@nl

prefLabel

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@en

Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

@nl

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AJPHEART.00783.2002

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American Journal of Physiology - Heart and Circulatory Physiology

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Bax ablation protects against myocardial ischemia-reperfusion injury in transgenic mice.

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Anna Tobar

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

Asher Shainberg

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Bernardo A Vidne

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Daniel Offen

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

Edith Hochhauser

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Hajime Otani

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Hannah Pannet

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Nilanjana Maulik

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Shaye Kivity

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Valeri Goldshtaub

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P2860

Molecular characterization of mitochondrial apoptosis-inducing factor

Bax-deficient mice with lymphoid hyperplasia and male germ cell death

Bcl-2 and Bax function independently to regulate cell death

Bcl-2 functions in an antioxidant pathway to prevent apoptosis

Toward antiapoptosis as a new treatment modality.

Apoptosis-related genes expressed in cardiovascular development and disease: an EST approach.

Using gene-targeted mice to investigate the pathophysiology of myocardial reperfusion injury.

Overexpression of the rat inducible 70-kD heat stress protein in a transgenic mouse increases the resistance of the heart to ischemic injury.

The mitochondrial death/life regulator in apoptosis and necrosis.

Bcl-2 decreases the free Ca2+ concentration within the endoplasmic reticulum.

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reperfusion injury