Independent modes of disease repair by AIM protein distinguished in AIM-felinized mice
Author:
Funder
MEXT | NINS | National Institute for Basic Biology
Japan Agency for Medical Research and Development
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-018-31580-6.pdf
Reference44 articles.
1. Miyazaki., T., Hirokami, Y., Matsuhashi, N., Takatsuka, H. & Naito, M. Increased susceptibility of thymocytes to apoptosis in mice lacking AIM, a novel murine macrophage-derived soluble factor belonging to the scavenger receptor cysteine-rich domain superfamily. J. Exp. Med. 189, 413–422 (1999).
2. Joseph, S. B. et al. LXR-dependent gene expression is important for macrophage survival and the innate immune response. Cell. 119, 299–309 (2004).
3. Valledor, A. F. et al. Activation of liver X receptors and retinoid X receptors prevents bacterial-induced macrophage apoptosis. Proc. Natl. Acad. Sci. USA 101, 17813–17818 (2004).
4. Arai, S. et al. A role of the apoptosis inhibitory factor AIM/Spα/Api6 in atherosclerosis development. Cell Metab. 1, 201–213 (2005).
5. Arai, S. et al. Obesity-associated autoantibody production requires AIM to retain IgM immune complex on follicular dendritic cells. Cell Rep. 3, 1187–1198 (2013).
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