2013 Fiscal Year Final Research Report
Analysis of signaling mechanisms for cellular response to low temperature in mammals
| Project/Area Number |
24657140
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
SATOH Takaya 大阪府立大学, 理学(系)研究科(研究院), 教授 (20251655)
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| Co-Investigator(Kenkyū-buntansha) |
TAKENAKA Nobuyuki 大阪府立大学, 大学院理学系研究科, 助教 (20610504)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | 低温刺激 / チロシンキナーゼ / ACK1 |
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| Research Abstract |
Body temperature in mammals is kept constant, contributing to the maintenance of stable environment around the cell. However, even in mammals, particular tissues such as skin and trachea are exposed to low temperature under ordinary conditions. Signaling mechanisms for cellular response to low temperature in these tissues remain obscure. In this study, we analyzed these signaling mechanisms, particularly the regulatory mechanisms and physiological function of the protein tyrosine kinase ACK1, in which tyrosine residues become phosphorylated following temperature shift down to 25 dgree in mammalian cultured cells.
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[Journal Article] Ras-related C3 botulinum toxin substrate 1 (RAC1) regulates glucose-stimulated insulin secretion via modulation of F-actin2013
Author(s)
S. Asahara, Y. Shibutani, K. Teruyama, H. Y. Inoue, Y. Kawada, H. Etoh, T. Matsuda, M. Kimura-Koyanagi, N. Hashimoto, M. Sakahara, W. Fujimoto, H. Takahashi, S. Ueda, T. Hosooka, T. Satoh, H. Inoue, M. Matsumoto, A. Aiba, M. Kasuga, and Y. Kido
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Journal Title
Diabetologia
Volume: 56 (05)
Pages: 1088-1097
DOI
Peer Reviewed
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