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Differences in the health-related quality of life in patients with asthma living in urban and rural areas in the Amur Region of Russian Federation

PloS one, 2023-11, Vol.18 (11), p.e0284683-e0284683

2023

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Cold temperature induces mucin hypersecretion from normal human bronchial epithelial cells in vitro through a transient receptor potential melastatin 8 (TRPM8)–mediated mechanism

Journal of allergy and clinical immunology, 2011-09, Vol.128 (3), p.626-634.e5

2011

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Interleukin-13 Induces Mucin 5AC Production Involving STAT6/SPDEF in Human Airway Epithelial Cells

Cell communication & adhesion, 2010-08, Vol.17 (4-6), p.83-92

2010

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The Degradation of Airway Epithelial Tight Junctions in Asthma Under High Airway Pressure Is Probably Mediated by Piezo-1

Frontiers in physiology, 2021-04, Vol.12, p.637790-637790

2021

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Human airway trypsin-like protease induces mucin5AC hypersecretion via a protease-activated receptor 2-mediated pathway in human airway epithelial cells

Archives of biochemistry and biophysics, 2013-07, Vol.535 (2), p.234-240

2013

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Oxidative stress mediates the disruption of airway epithelial tight junctions through a TRPM2-PLCγ1-PKCα signaling pathway

International journal of molecular sciences, 2013-04, Vol.14 (5), p.9475-9486

2013

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The chitinase-like protein YKL-40 increases mucin5AC production in human bronchial epithelial cells

Experimental cell research, 2013-11, Vol.319 (18), p.2866-2873

2013

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Retraction Note: MiR-146a negatively regulates neutrophil elastase-induced MUC5AC secretion from 16HBE human bronchial epithelial cells

Molecular and cellular biochemistry, 2024-12, Vol.479 (12), p.3491-3491

2024

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The effect of quercetin on human neutrophil elastase‐induced mucin5AC expression in human airway epithelial cells

International immunopharmacology, 2012-10, Vol.14 (2), p.195-201

2012

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Ezrin/Exocyst Complex Regulates Mucin 5AC Secretion Induced by Neutrophil Elastase in Human Airway Epithelial Cells

Cellular physiology and biochemistry, 2015-01, Vol.35 (1), p.326-338

2015

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Regulator of G-protein signaling 2 inhibits acid-induced mucin5AC hypersecretion in human airway epithelial cells

Respiratory physiology & neurobiology, 2013-01, Vol.185 (2), p.265-271

2013

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The degradation of airway tight junction protein under acidic conditions is probably mediated by transient receptor potential vanilloid 1 receptor

Bioscience reports, 2013-10, Vol.33 (5)

2013

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The Cosmc-mediated effects of neutrophil elastase on T antigen expression in BEAS-2B cells

Respiratory physiology & neurobiology, 2020-10, Vol.281, p.103496-103496, Article 103496

2020

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Effect of epithelium ATP release on cyclic pressure-induced airway mucus secretion

Bioscience reports, 2014-02, Vol.34 (1)

2014

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Secretoneurin Induces Airway Mucus Hypersecretion by Enhancing the Binding of EGF to NRP1

Cellular physiology and biochemistry, 2014-01, Vol.33 (2), p.446-456

2014

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Nicotine suppresses inflammatory factors in HBE16 airway epithelial cells after exposure to cigarette smoke extract and lipopolysaccharide

Translational research : the journal of laboratory and clinical medicine, 2010-12, Vol.156 (6), p.326-334

2010

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Vaccine Prophylaxis of Pneumococcal Infections in Children under Conditions of Severe Flood in the Amur River Basin

Interdisciplinary perspectives on infectious diseases, 2019, Vol.2019 (2019), p.1-9

2019

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The Expression and Pharmacological Characterization of Nicotinic Acetylcholine Receptor Subunits in HBE16 Airway Epithelial Cells

Cell biochemistry and biophysics, 2012-04, Vol.62 (3), p.421-431

2012

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Transient receptor potential vanilloid 1 receptors mediate acid-induced mucin secretion via Ca2+ influx in human airway epithelial cells

Journal of biochemical and molecular toxicology, 2012-05, Vol.26 (5), p.179-186

2012

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MicroRNA-155 regulates lipopolysaccharide-induced mucin 5AC overproduction via a suppressor of cytokine signaling 1-mediated mechanism in human bronchial epithelial cells

Respiratory physiology & neurobiology, 2019-06, Vol.264, p.12-18

2019

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The role of the XBP-1/AGR2 signaling pathway in the regulation of airway Mucin5ac hypersecretion under hypoxia

Experimental cell research, 2019-09, Vol.382 (1), p.111442-111442, Article 111442

2019

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Cold-inducible RNA-binding protein mediates airway inflammation and mucus hypersecretion through a post-transcriptional regulatory mechanism under cold stress

The international journal of biochemistry & cell biology, 2016-09, Vol.78, p.335-348

2016

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Neutrophil elastase induces MUC5AC secretion via protease-activated receptor 2

Molecular and cellular biochemistry, 2013-05, Vol.377 (1-2), p.75-85

2013

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Effects of scutellarin on MUC5AC mucin production induced by human neutrophil elastase or interleukin 13 on airway epithelial cells

Journal of Korean Medical Science, 2011, 26(6), 152, pp.778-784

2011

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Bronchial inflammatory profile in interferon-gamma-mediated immune response in asthma patients during airway response to cold stimulus

Frigid Zone Medicine (Warsaw. Online), 2022-12, Vol.2 (4), p.244-250

2022

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Differences in the health-related quality of life in patients with asthma living in urban and rural areas in the Amur Region of Russian Federation

Cold temperature induces mucin hypersecretion from normal human bronchial epithelial cells in vitro through a transient receptor potential melastatin 8 (TRPM8)–mediated mechanism

Interleukin-13 Induces Mucin 5AC Production Involving STAT6/SPDEF in Human Airway Epithelial Cells

The Degradation of Airway Epithelial Tight Junctions in Asthma Under High Airway Pressure Is Probably Mediated by Piezo-1

Human airway trypsin-like protease induces mucin5AC hypersecretion via a protease-activated receptor 2-mediated pathway in human airway epithelial cells

Oxidative stress mediates the disruption of airway epithelial tight junctions through a TRPM2-PLCγ1-PKCα signaling pathway

The chitinase-like protein YKL-40 increases mucin5AC production in human bronchial epithelial cells

Retraction Note: MiR-146a negatively regulates neutrophil elastase-induced MUC5AC secretion from 16HBE human bronchial epithelial cells

The effect of quercetin on human neutrophil elastase‐induced mucin5AC expression in human airway epithelial cells

Ezrin/Exocyst Complex Regulates Mucin 5AC Secretion Induced by Neutrophil Elastase in Human Airway Epithelial Cells

Regulator of G-protein signaling 2 inhibits acid-induced mucin5AC hypersecretion in human airway epithelial cells

The degradation of airway tight junction protein under acidic conditions is probably mediated by transient receptor potential vanilloid 1 receptor

The Cosmc-mediated effects of neutrophil elastase on T antigen expression in BEAS-2B cells

Effect of epithelium ATP release on cyclic pressure-induced airway mucus secretion

Secretoneurin Induces Airway Mucus Hypersecretion by Enhancing the Binding of EGF to NRP1

Nicotine suppresses inflammatory factors in HBE16 airway epithelial cells after exposure to cigarette smoke extract and lipopolysaccharide

Vaccine Prophylaxis of Pneumococcal Infections in Children under Conditions of Severe Flood in the Amur River Basin

The Expression and Pharmacological Characterization of Nicotinic Acetylcholine Receptor Subunits in HBE16 Airway Epithelial Cells

Transient receptor potential vanilloid 1 receptors mediate acid-induced mucin secretion via Ca2+ influx in human airway epithelial cells

MicroRNA-155 regulates lipopolysaccharide-induced mucin 5AC overproduction via a suppressor of cytokine signaling 1-mediated mechanism in human bronchial epithelial cells

The role of the XBP-1/AGR2 signaling pathway in the regulation of airway Mucin5ac hypersecretion under hypoxia

Cold-inducible RNA-binding protein mediates airway inflammation and mucus hypersecretion through a post-transcriptional regulatory mechanism under cold stress

Neutrophil elastase induces MUC5AC secretion via protease-activated receptor 2

Effects of scutellarin on MUC5AC mucin production induced by human neutrophil elastase or interleukin 13 on airway epithelial cells

Bronchial inflammatory profile in interferon-gamma-mediated immune response in asthma patients during airway response to cold stimulus

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