S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

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S100A12 as a marker of worse cardiac output and mortality in pulmonary hypertension.

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S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

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2012 nî lūn-bûn

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2012年の論文

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S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

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Blanca Camoretti-Mercado

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Eltayeb Karrar

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Luis Nuñez

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Marion A Hofmann Bowman

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P2860

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

Antigen-sensitized CD4+CD62Llow memory/effector T helper 2 cells can induce airway hyperresponsiveness in an antigen free setting

Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock

A role for the receptor for advanced glycation end products in idiopathic pulmonary fibrosis

The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system

Changing the conformation state of cytochrome b558 initiates NADPH oxidase activation: MRP8/MRP14 regulation.

S100A8 chemotactic protein is abundantly increased, but only a minor contributor to LPS-induced, steroid resistant neutrophilic lung inflammation in vivo.

Biomarker discovery in asthma-related inflammation and remodeling.

Airway hyperresponsiveness in asthma: not just a matter of airway inflammation

The RAGE axis: a fundamental mechanism signaling danger to the vulnerable vasculature

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10.4172/2155-6121.S1-007

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Suppl 1

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S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

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S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

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