Analysis of relationship between pathogenesis and ER stress sensor-derived small peptides produced in response to ER stress

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K18395
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: Hiroshima University
• Principal Investigator: Matsuhisa Koji 広島大学, 医歯薬保健学研究科(医), 寄附講座助教 (60735299)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 小胞体ストレス / 神経変性疾患

Outline of Final Research Achievements

Previous studies have shown the robust involvement of endoplasmic reticulum (ER) dysfunctions and ER stress in the development of various diseases such as neurodegenerative disorders. However, the molecular entities linking ER stress with the pathogenesis of these diseases have been unexplored. We identified the small peptide fragments generated from ER stress sensors ATF6 and OASIS family members in an ER stress-dependent manner. The fragments are hydrophobic, highly aggregable and form fibrils. The small peptides also promote the fibrilization of amyloid β. These data indicate that the small peptides might be key molecules linking between ER stress and the pathogenesis of neurodegenerative diseases

Free Research Field

生化学、薬学