Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury. - Wikidata - awgldk - TriplyDB

Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury.

Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury.

http://www.wikidata.org/entity/Q33726917

about

IL-6 protects against hyperoxia-induced mitochondrial damage via Bcl-2-induced Bak interactions with mitofusins A1/Bfl-1 in leukocyte development and cell death Regulation of Bcl-xL expression in lung vascular smooth muscle Gene expression patterns induced at different stages of rhinovirus infection in human alveolar epithelial cells.Effects of age on the synergistic interactions between lipopolysaccharide and mechanical ventilation in mice.Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development.Role of CCR5 in IFN-gamma-induced and cigarette smoke-induced emphysema.The chitinase-like proteins breast regression protein-39 and YKL-40 regulate hyperoxia-induced acute lung injury.Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung.p21Cip1 protection against hyperoxia requires Bcl-XL and is uncoupled from its ability to suppress growth The microRNA-21-PDCD4 axis prevents type 1 diabetes by blocking pancreatic beta cell death.Exposure to high concentrations of inspired oxygen does not worsen lung injury after cardiac arrest.Adiponectin expression and the cardioprotective role of the vitamin D receptor activator paricalcitol and the angiotensin converting enzyme inhibitor enalapril in ApoE-deficient mice.Adenovirus-mediated transfer of the SOCS-1 gene to mouse lung confers protection against hyperoxic acute lung injury.NALP-3 inflammasome silencing attenuates ceramide-induced transepithelial permeability.Increased hyperoxia-induced lung injury in nitric oxide synthase 2 null mice is mediated via angiopoietin 2.DHA suppresses chronic apoptosis in the lung caused by perinatal inflammation Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management.Update in critical care 2005.Deletion of P2X7 attenuates hyperoxia-induced acute lung injury via inflammasome suppression Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells STAT3 and suppressor of cytokine signaling 3: potential targets in lung inflammatory responses.Developmental regulation of NO-mediated VEGF-induced effects in the lung.Pulmonary natural killer T cells play an essential role in mediating hyperoxic acute lung injury.NLRP3 deletion protects from hyperoxia-induced acute lung injury Beta-catenin in the fibroproliferative response to acute lung injury Bcl-X(L) is the primary mediator of p21 protection against hyperoxia-induced cell death The inflammasome mediates hyperoxia-induced alveolar cell permeability.IL-6 cytoprotection in hyperoxic acute lung injury occurs via PI3K/Akt-mediated Bax phosphorylation.Hyperoxia causes angiopoietin 2-mediated acute lung injury and necrotic cell death A paradoxical protective role for the proinflammatory peptide substance P receptor (NK1R) in acute hyperoxic lung injury IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.BCL2A1: the underdog in the BCL2 family.Oxidative stress modulates the expression of genes involved in cell survival in ΔF508 cystic fibrosis airway epithelial cells.PUMA inactivation protects against oxidative stress through p21/Bcl-XL inhibition of bax death.Interleukin-4 induces lipogenesis in porcine endothelial cells, which in turn is critical for induction of protection against complement-mediated injury.Hyperoxic acute lung injury and ventilator-induced/associated lung injury: new insights into intracellular signaling pathways.Endogenous IL-11 signaling is essential in Th2- and IL-13-induced inflammation and mucus production IL-6 cytoprotection in hyperoxic acute lung injury occurs via suppressor of cytokine signaling-1-induced apoptosis signal-regulating kinase-1 degradation.

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Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury.

http://www.wikidata.org/entity/Q33726917

description

2005 nî lūn-bûn

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2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2005 թվականի ապրիլին հրատարակված գիտական հոդված

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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年學術文章

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Bcl-2-related protein A1 is an ...... n hyperoxic acute lung injury.

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Journal of Clinical Investigation

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Bcl-2-related protein A1 is an ...... n hyperoxic acute lung injury.

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Aaron B Waxman

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Bing Ma

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Chuan Hua He

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Holger Link

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Jack A Elias

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Keiichi I Nakayama

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Keiko Nakayama

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Mei Zhong

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Morgan E Rabach

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Qingsheng Chen

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P2860

Vascular endothelial growth factor (VEGF) upregulates BCL-2 and inhibits apoptosis in human and murine mammary adenocarcinoma cells

MCP-1 (CCL2) protects human neurons and astrocytes from NMDA or HIV-tat-induced apoptosis

The prosurvival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappaB that blocks TNFalpha-induced apoptosis

A1 functions at the mitochondria to delay endothelial apoptosis in response to tumor necrosis factor

Characterization of A1, a novel hemopoietic-specific early-response gene with sequence similarity to bcl-2

Endothelial cell death induced by tumor necrosis factor-alpha is inhibited by the Bcl-2 family member, A1

VEGF protects bovine aortic endothelial cells from TNF-alpha- and H2O2-induced apoptosis via co-modulatory effects on p38-and p42/p44-CCDPK signaling.

Hyperoxia-induced cell death in the lung--the correlation of apoptosis, necrosis, and inflammation.

Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions.

Evaluation of survival data and two new rank order statistics arising in its consideration.

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1039-1048

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10.1172/JCI23004

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4

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115

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Robert J. Homer

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15841185

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