TAKAHASHI Kenichi

写真a

Affiliation

Hospital  Internal MedichineⅠ 

Research Interests 【 display / non-display

  • 消化器病

Graduating School 【 display / non-display

  •  
    -
    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

  • 2018.10
    -
    Now

    Akita University   Hospital   Internal MedichineⅠ   Assistant Professor  

 

Research Achievements 【 display / non-display

    ◆Original paper【 display / non-display

  • 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

    DOI

  • ◆Introduction and explanation【 display / non-display

  • 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

  • ◆Other【 display / non-display

  • 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>

    DOI