Function analysis of endoplasmic reticulum stress inducible protein Herp focused on a calcium release in endoplasmic reticulum

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460100
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pharmacology in pharmacy
• Research Institution: Nihon Pharmaceutical University (2015-2016); Iwate Medical University (2014)
• Principal Investigator: MAEDA Tomoji 日本薬科大学, 薬学部, 准教授 (60303294)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: Herp / 小胞体 / 小胞体関連分解 / カルシウム放出 / ユビキチン / プロテアソーム

Outline of Final Research Achievements

Homocysteine-inducible endoplasmic reticulum protein (Herp) is an endoplasmic reticulum stress-inducible membrane protein that is involved in endoplasmic reticulum-associated degradation (ERAD). Herp expression is maintained at low levels through a strict regulatory mechanism. However, the mechanisms through which Herp is maintained at low levels remain unclear. Here, we showed that Herp degradation was also regulated through ubiquitination mechanisms or a ubiquitin-independent pathway. In addition, we found that Herp is involved in calcium release in endoplasmic reticulum via inositol 1,4,5 triphosphate (IP3) receptor. These results suggested that Herp is involved in several important functions, such as ERAD and calcium release, its levels may be strictly regulated by degradation through multiple pathways in response to various physiological conditions.

Free Research Field

医療薬学