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Affiliation |
Hospital Internal MedichineⅠ |
Graduating School 【 display / non-display 】
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-2010.03
Akita University Faculty of Medicine Graduated
Graduate School 【 display / non-display 】
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-2018.03
Akita University Graduate School, Division of Medicine Doctor's Course Completed
Campus Career 【 display / non-display 】
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2018.10-Now
Akita University Hospital Internal MedichineⅠ Assistant Professor
Research Achievements 【 display / non-display 】
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Disruption of small GTPase Rab7 exacerbates the severity of acute pancreatitis in experimental mouse models.
, Mashima H, Miura K, Maeda D, Goto A, Goto T, Sun-Wada GH, Wada Y, Ohnishi H.
Scientific Reports 2017.06 [Refereed]
Research paper (journal) Domestic Co-author
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Participation of intracellular vesicular trafficking in acute pancreatitis
suizo ( japan pancreas society ) 33 ( 4 ) 723 - 729 2018.08
Introduction and explanation (scientific journal) Single author
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Participation of intracellular vesicular trafficking in acute pancreatitis
TAKAHASHI Kenichi, MASHIMA Hirosato, OHNISHI Hirohide
Suizo ( Japan Pancreas Society ) 33 ( 4 ) 723 - 729 2018
<p>Pancreatic acinar cells synthesize a variety of digestive enzymes and secrete them into the pancreatic duct. Intracellular vesicle transport mechanisms play important roles in maintaining these functions. Exocytosis, autophagy and endocytosis are representative of intracellular vesicle trafficking in pancreatic acinar cells. These intracellular vesicular trafficking systems are mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins, autophagy-related genes and the Ras-related GTP-binding protein Rab family. Recent studies demonstrated that defects in intracellular vesicular trafficking systems including exocytosis, autophagy and endocytosis are involved in the onset and progression of acute pancreatitis. These intracellular trafficking pathways are closely related to each other. Therefore, in order to elucidate the pathophysiological mechanisms of acute pancreatitis, it is important to investigate the interactions as well as the participation of each pathway in the onset and progression of acute pancreatitis.</p>