Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels. - Wikidata - awgldk - TriplyDB

Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels.

Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels.

http://www.wikidata.org/entity/Q34876449

about

Targeting mitochondrial reactive oxygen species as novel therapy for inflammatory diseases and cancers The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases Redox regulation of mitochondrial biogenesis Reactive oxygen species in inflammation and tissue injury Physiological roles of mitochondrial reactive oxygen species A comparative study on inhibition of total astragalus saponins and astragaloside IV on TNFR1-mediated signaling pathways in arterial endothelial cells Mitochondria, endothelial cell function, and vascular diseases.Mitochondrial ion channels/transporters as sensors and regulators of cellular redox signaling.Sessile alveolar macrophages communicate with alveolar epithelium to modulate immunity.Mitochondrial Ca²+ and ROS take center stage to orchestrate TNF-α-mediated inflammatory responses Monocyte Tumor Necrosis Factor-α-Converting Enzyme Catalytic Activity and Substrate Shedding in Sepsis and Noninfectious Systemic Inflammation.Inflammation alters regional mitochondrial Ca²+ in human airway smooth muscle cells.An in vitro model for the assessment of stem cell fate following implantation within the infarct microenvironment identifies ISL-1 expression as the strongest predictor of c-Kit(+) cardiac progenitor cells' therapeutic potential.A role for cGMP in inducible nitric-oxide synthase (iNOS)-induced tumor necrosis factor (TNF) α-converting enzyme (TACE/ADAM17) activation, translocation, and TNF receptor 1 (TNFR1) shedding in hepatocytes.Mesenchymal stem cells suppress CaN/NFAT expression in the pulmonary arteries of rats with pulmonary hypertension Mesenchymal stem cell-conditioned media suppresses inflammation-associated overproliferation of pulmonary artery smooth muscle cells in a rat model of pulmonary hypertension.Shedding of the tumor necrosis factor (TNF) receptor from the surface of hepatocytes during sepsis limits inflammation through cGMP signaling.Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy.Mitochondria and endothelial function FXYD5 Protein Has a Pro-inflammatory Role in Epithelial Cells.Mechanical ventilation causes pulmonary mitochondrial dysfunction and delayed alveolarization in neonatal mice.TNFR1/phox interaction and TNFR1 mitochondrial translocation Thwart silica-induced pulmonary fibrosis.Mitochondria in lung diseases.Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes.Live imaging of the lung.Mitochondria-meditated pathways of organ failure upon inflammation.The pulmonary endothelium in acute respiratory distress syndrome: insights and therapeutic opportunities.Macrophage-epithelial interactions in pulmonary alveoli.Roles of extracellular nucleotides and P2 receptors in ectodomain shedding.Ramalin inhibits VCAM-1 expression and adhesion of monocyte to vascular smooth muscle cells through MAPK and PADI4-dependent NF-kB and AP-1 pathways.Mitochondrial Dysfunction in Airway Disease.Neutralization of MMP-2 and TNFR1 Regulates the Severity of S. aureus-Induced Septic Arthritis by Differential Alteration of Local and Systemic Proinflammatory Cytokines in Mice.Cadherin selectivity filter regulates endothelial sieving properties.Mitochondrial transfer from bone-marrow-derived stromal cells to pulmonary alveoli protects against acute lung injury.Real-time imaging reveals endothelium-mediated leukocyte retention in LPS-treated lung microvessels.The tubule pathology of septic acute kidney injury: a neglected area of research comes of age.The role of mitochondrial permeability transition pore in regulating the shedding of the platelet GPIbα ectodomain.A novel ratiometric emission probe for Ca2+ in living cells.Tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability: role of intrinsic apoptotic signaling.Tumor necrosis factor receptor 1 gain-of-function mutation aggravates nonalcoholic fatty liver disease but does not cause insulin resistance in a murine model.

P2860

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P2860

Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels.

http://www.wikidata.org/entity/Q34876449

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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name

Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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type

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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Activation of TNFR1 ectodomain ...... on in mouse lung microvessels.

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David J Rowlands

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Jahar Bhattacharya

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Jens Lindert

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Memet T Emin

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Mohammad Naimul Islam

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Nilufar Inamdar

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Sadiqa K Quadri

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Shonit R Das

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Sunita Bhattacharya

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Vadim S Ten

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P2860

Ca(2+) transfer from the ER to mitochondria: when, how and why

Investigating mitochondrial redox potential with redox-sensitive green fluorescent protein indicators

Immunity, Inflammation, and Cancer

A metalloproteinase disintegrin that releases tumour-necrosis factor-alpha from cells

TNF-R1 signaling: a beautiful pathway

Red blood cells induce hypoxic lung inflammation

Connexin 43 mediates spread of Ca2+-dependent proinflammatory responses in lung capillaries.

Calcium oscillations increase the efficiency and specificity of gene expression

Mitochondrial complex III is required for hypoxia-induced ROS production and cellular oxygen sensing

The pathophysiology and treatment of sepsis

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