■ Book and thesis
1.
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2022/07
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Article
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A Splice Switch in SIGIRR Causes a Defect of IL-37-Dependent Anti-Inflammatory Activity in Cystic Fibrosis Airway Epithelial Cells International Journal of Molecular Sciences 23(14),pp.7743 (Collaboration)
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2.
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2022/06
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Article
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Metformin suppresses epithelial sodium channel hyperactivation and its associated phenotypes in a mouse model of obstructive lung diseases Journal of Pharmacological Sciences 149(2),pp.37-45 (Collaboration)
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3.
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2020/05
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Article
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Higher Blood Uric Acid in Female Humans and Mice as a Protective Factor Against Pathophysiological Decline of Lung Function Antioxidants 9(5),pp.387 (Collaboration)
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4.
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2020/04
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Article
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Intratracheal GLP-1 receptor agonist treatment up-regulates mucin via p38 and exacerbates emphysematous phenotype in mucus hypersecretory obstructive lung diseases Biochemical and Biophysical Research Communications 524(2),pp.332-339 (Collaboration)
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5.
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2020/01
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Article
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Azithromycin inhibits constitutive airway epithelial sodium channel activation in vitro and modulates downstream pathogenesis in vivo Biological and Pharmaceutical Bulletin 43(4),pp.725-730 (Collaboration)
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6.
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2019/03
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Article
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Curcumin down-regulates toll-like receptor-2 gene expression and function in human cystic fibrosis bronchial epithelial cells Biological and Pharmaceutical Bulletin 42(3),pp.489-495 (Collaboration)
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7.
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2019/02
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Article
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Integrative expression analysis identifies a novel interplay between CFTR and linc-SUMF1-2 that involves CF-associated gene dysregulation. Biochemical and Biophysical Research Communications 509(2),pp.521-528 (Collaboration)
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8.
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2018/11
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Other
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Smoking Status Among Pharmacy Students and the Environment that They Started Smoking Journal of Kyushu Pharmacy pp.7-11 (Collaboration)
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9.
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2018/01
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Article
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CFTR and ENaC controls cystic fibrosis-associated mucus hypersecretory phenotype through a novel splice switch of zinc importer ZIP2/SLC39A2 EBioMedicine 27,pp.304-316 (Collaboration)
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10.
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2014/06
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Article
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Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1Receptor-Related
Molecule (SIGIRR) Expression by Suppressing Sp1 via TLR4-p38 pathway in monocytes and neutrophils Journal of Biological Chemistry 289(26),pp.18097-18109 (Collaboration)
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11.
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2013/09
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Article
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Increased IL-17C production by the TLR3 ligand poly(I:C) in primary cystic fibrosis airway epithelial cells Pediatric Pulmonology (Collaboration)
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12.
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2012/04
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Article
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Synergism between Interleukin-17 and Toll-like receptor 2 and 4 Signals to Induce IL-8 Expression in Cystic Fibrosis Airway Epithelial Cells Journal of Pharmacological Sciences 118(4),pp.512-520 (Collaboration)
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13.
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2009/11
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Article
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Calreticulin positively regulates the expression and function of epithelial sodium channel Experimental Cell Research 315(19),pp.3294-3300 (Collaboration)
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14.
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2008/03
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Article
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MUC1 mucin is a negative regulator of toll-like receotor signaling Americal Journal of Respiratory Cell and Molecular Biology 38,pp.263-268 (Collaboration)
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15.
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2008/01
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Article
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Phosphatidic acid metabolism regulates the intracellular trafficking and retrotranslocation of CFTR Biochimica et Biophysica Acta 1783,pp.153-162 (Collaboration)
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16.
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2006/05
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Article
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Calreticulin negatively regulates the cell surface expression of cystic fibrosis transmembrane conductance regulator Journal of Biological Chemistry 281,pp.12841-12848 (Collaboration)
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17.
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2004/08
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Article
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Characterization of the trafficking pathway of cystic fibrosis transmembrane conductance regulator in baby hamster kidney cells Journal of Pharmacological Sciences 95(4),pp.471-475 (Collaboration)
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Display 5 items
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Display all(17)
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■ Academic conference presentation
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■ Academic background
1. |
2000/04~2004/03
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Faculty of Pharmaceutical Science, Kumamoto University, Graduated,
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2. |
2004/04~2006/03
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〔Master Course〕, Graduate School, Division of Pharmaceutical Sciences, Kumamoto University, Completed,
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3. |
2006/04~2009/03
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〔Doctorial Course〕, Graduate School, Division of Pharmaceutical Sciences, Kumamoto University, Completed,
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■ Business career
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■ researchmap Researcher code
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■ Research topic, funded research, and department laboratory expense
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■ E-Mail Address
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■ Present specialized field
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■ Department laboratory expense researcher number
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