Elucidation of the mechanism underlying apoptosis-induced compensatory proliferation using a murine model
Project/Area Number |
25670167
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Pathological medical chemistry
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Research Institution | Toho University (2014) Juntendo University (2013) |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 細胞死 / cFLIP / アポトーシス / ネクロプトーシス / 腸炎 / X染色体不活性化 / 代償性増殖 / ノックインマウス / RegIII / X染色体 / マイクロアレイ / Crisper/Cas9 / cFLIPs / トランスジェニックマウス |
Outline of Final Research Achievements |
Apoptotic cells might produce growth factors that subsequently induce proliferation, which is referred to as compensatory proliferation. The aim of the study is to identify growth factors released from dying cells and elucidate the mechanisms underlying compensatory proliferation. We generated mice that harbored cFLIPs gene at a locus on X chromosome. Intestinal epithelial cells of cFLIPs KI mice underwent apoptosis, however, female cFLIPs KI mice were born and developed without abnormality, and fertile. To identify candidate genes that are potentially involved in proliferation, we performed genome-wide transcriptome analysis using intestines of cFLIPs KI embryos and we found that RegIIIb and RegIIIg involved in tissue repair were significantly elevated in the intestine of cFLIPs KI embryos compared to wild-type embryos. Now, we are going to generate mice lacking both RegIIIb and RegIIIg to elucidate a role for these genes in compensatory proliferation.
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Report
(3 results)
Research Products
(29 results)
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[Journal Article] Antibody against chromatin assembly factor-1 is a novel autoantibody specifically recognized in systemic lupus erythematosus.2014
Author(s)
Doe, K., K. Nozawa, K. Hiruma, Y. Yamada, Y. Matsuki, S. Nakano, M. Ogasawara, H. Nakano, T. Ikeda, T. Ikegami, M. Fujishiro, M. Kawasaki, K. Ikeda, H. Amano, S. Morimoto, H. Ogawa, K. Takamori, I. Sekigawa, and Y. Takasaki.
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Journal Title
Lupus
Volume: 23
Pages: 1031-1041
DOI
Related Report
Peer Reviewed
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[Journal Article] The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6.2014
Author(s)
1. Nagashima, H., Okuyama, Y., Asao, A., Kawabe, T., Yamaki, S., Nakano, H., Croft, M., Ishii, N., and So, T.
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Journal Title
Nat Immunol
Volume: 15
Pages: 449-456
DOI
Related Report
Peer Reviewed
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[Journal Article] Disruption of Tumor Necrosis Factor Receptor Associated Factor 5 Exacerbates Pressure Overload Cardiac Hypertrophy and Fibrosis.2014
Author(s)
Bian, Z., Dai, J., Nakano, H., Guan, H., Yuan, Y., Gan, L., Zhou, H., Zong, J., Zhang, Y., Li, F., Yan, L., Shen, D., Li, H., and Tang, Q.
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Journal Title
J Cell Biochem
Volume: 115
Pages: 349-358
DOI
Related Report
Peer Reviewed
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[Journal Article] Tumor Necrosis Factor Receptor Associated Factor 5 is an Essential Mediator of Ischemic Brain Infarction.2013
Author(s)
Wang, L., Lu, Y., Guan, H., Jiang, D., Guan, Y., Zhang, X., Nakano, H., Zhou, Y., Zhang, Y., Yang, L., and Li, H.
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Journal Title
J Neurochem
Volume: 126
Pages: 400-414
DOI
Related Report
Peer Reviewed
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[Journal Article] Hyperosmotic stress regulates the distribution and stability of myocardin-related transcription factor, a key modulator of the cytoskeleton.2013
Author(s)
Ly, D. L., Waheed, F., Lodyga, M., Speight, P., Masszi, A., Nakano, H., Hersom, M., Pedersen, S. F., Szaszi, K., and Kapus, A.
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Journal Title
Am J Physiol Cell Physiol
Volume: 304
Pages: C115-127
DOI
Related Report
Peer Reviewed
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