Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury - Test2 - elhamkhani - TriplyDB

Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

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The Matrikine Acetylated Proline-Glycine-Proline Couples Vascular Inflammation and Acute Cardiac Rejection.SOCS molecules: the growing players in macrophage polarization and function.Deficiency of NALP3 Signaling Impairs Liver Regeneration After Partial Hepatectomy.Lack of SOCS3 increases LPS-induced murine acute lung injury through modulation of Ly6C(+) macrophages.Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway.Fine chalk dust induces inflammatory response via p38 and ERK MAPK pathway in rat lung.Recent advances in our understanding of the mechanisms of late lung development and bronchopulmonary dysplasia.Downregulation of Paralemmin-3 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating Inflammatory Response and Inhibiting Formation of TLR4/MyD88 and TLR4/TRIF Complexes.Epithelial disruption of Gab1 perturbs surfactant homeostasis and predisposes mice to lung injuries.Landscape of transcription and long non-coding RNAs reveals new insights into the inflammatory and fibrotic response following ventilator-induced lung injury.

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Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

http://www.wikidata.org/entity/Q40471161

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2016 nî lūn-bûn

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2016年の論文

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年學術文章

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2016年學術文章

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2016年學術文章

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Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

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Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

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Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

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AJPLUNG.00281.2016

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American Journal of Physiology - Lung Cellular and Molecular Physiology

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Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury

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Amit Gaggar

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Chenglong Li

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

Etty N Benveniste

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Hao Yu

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

Jiping Zhao

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Pui-Kai Li

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Sara A Gibson

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Shi Wei

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Xin Xu

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P2860

Pressure-controlled versus volume-controlled ventilation for acute respiratory failure due to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS)

LPS induces CD40 gene expression through the activation of NF-kappaB and STAT-1alpha in macrophages and microglia

Screening approaches to generating STAT inhibitors: Allowing the hits to identify the targets

Lung inflammation, injury, and proliferative response after repetitive particulate hexavalent chromium exposure

Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium

STAT-3 regulates surfactant phospholipid homeostasis in normal lung and during endotoxin-mediated lung injury

Incidence and outcomes of acute lung injury

A novel small molecule, LLL12, inhibits STAT3 phosphorylation and activities and exhibits potent growth-suppressive activity in human cancer cells.

SOCS1 and SOCS3 in the control of CNS immunity

The innate immune response of the respiratory epithelium.

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