Functional analysis of Alivin1/Amigo2
Project/Area Number |
16500253
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | Tokyo metropolitan organization for Medical Research |
Principal Investigator |
ONO Tomio Tokyo metropolitan organization for Medical Research, The Tokyo metropolitan institute of medical science, Research Scientist (60231239)
|
Project Period (FY) |
2004 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,970,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | apoptosis / Alivin / neuronal activity / Alzheimer's disease / neuronal cell death / cerebellar granule neurons / leucine rich repeat / immunoglobulin |
Research Abstract |
Alivin1/Amigo2 is a neuronal activity-dependent gene that is a potential therapeutic target for neurodegenerative diseases. This gene was originally discovered by us (1) and has been shown to be involved in neuronal activity-dependent suppression of apoptosis, cell adhesion, migration, and carcinogenesis. Alivin1 encodes a transmembrane protein that has 6.5 times leucine-rich repeats (LRR) and one immunoglobulin (IG) domain. The encoded protein is assumed to interact with its binding partner (s) through these LRR and IG domains and involve in the signal transduction (s) for survival. In order to study biological functions of alivin 1 in mice, we generated the knockout mouse line. Open-field tests were carried out twice with a week interval using the same subjects of alivin1(-/-) and wild type mice (WT). The primary open-field tests showed that the per cent time spent in the central area of the field of alivin1 (-/-) mice was larger than that of WT, suggesting that alivin 1 (-/-) mice have reduced fear and anxiety compared to WT. The comparison between the results of the primary and the secondary tests showed that the locomotor activity of alivin1 (-/-) mice under the familiar environment was larger than that of WT. Alivin1 (-/-) mice kept in their home cages also showed higher locomotor activity than WT. These results suggest that deficiency in alivin1 is associated with enhanced locomotor activity and reduced fear and anxiety. (1) Ono et al.J.Neurosci.23, 5887-5896, 2003.
|
Report
(5 results)
Research Products
(10 results)
-
[Journal Article] Hippocalcin protects hippocampal neurons against excitotoxin damage by enhancing calcium extrusion.2007
Author(s)
Masuo,Y., Ogura,A., Kobayashi,M., Masaki,T., Furuta,Y., Ono,T., Takamatsu,K.
-
Journal Title
Neuroscience 145
Pages: 495-504
Description
「研究成果報告書概要(和文)」より
Related Report
Peer Reviewed
-
[Journal Article] Hippocalcin protects hippocampal neurons against excitotoxin damage by enhancing calcium extrusion2007
Author(s)
Masuo, Y., Ogura, A., Kobayashi, M., Masaki, T., Furuta, Y., Ono, T., Takamatsu, K.
-
Journal Title
Neuroscience 145
Pages: 495-504
Description
「研究成果報告書概要(欧文)」より
Related Report
-
-
-
-
[Presentation] Mice deficient in alivin1/amigo2 show enhanced locomotor activity and reduced fear and anxiety.2008
Author(s)
Ono,T., Akamatsu,N., Shitara,H., Ishii,R., Taya,C., Yamada,I., Shibukawa,Y., Kushida,T., Furuse,T., Watabe,K., Wakana,S., Yonekawa,H.
Organizer
The 22nd International Mammalian Genome Conference(IMGC2008)
Place of Presentation
Prague, Czech
Description
「研究成果報告書概要(和文)」より
Related Report
-
[Presentation] Mice deficient in alivin1/amigo2 show enhanced locomotor activity and reduced fear and anxiety2008
Author(s)
Ono, T., Akamatsu, N., Shitara, H., Ishii, R., Taya, C., Yamada, I., Shibukawa, Y., Kushida, T., Furuse, T., Watabe, K., Wakana, S., Yonekawa, H.
Organizer
The 22nd International Mammalian Genome Conference(IMGC2008)
Place of Presentation
Prague, Czech
Description
「研究成果報告書概要(欧文)」より
Related Report
-
-
-