The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Calpain Mediates Excitotoxic DNA Fragmentation via Mitochondrial Pathways in Adult Brains
Open accessAbstract
Calpain has been implicated in excitotoxic neurode-generation, but its mechanism of action particularly in adult brains remains unclear. We generated mutant mice lacking or overexpressing calpastatin, the only solely calpain-specific inhibitor ever identified or synthesized. Modulation of calpastatin expression caused no defect in the mice under normal conditions, indicating that calpastatin functions as a negative regulator of calpain only under pathological conditions. Kainate-evoked excitotoxicity in hippocampus resulted in proteolytic activation of a proapoptotic Bcl-2 subfamily member (Bid), nuclear translocation of mitochondria-derived DNA fragmentation factors (apoptosis-inducing factor and endonuclease G), DNA fragmentation, and nuclear condensation in pyramidal neurons. These apoptotic responses were significantly augmented by calpastatin deficiency. Consistently calpastatin overexpression suppressed them. No evidence of caspase-3 activation was detected. Our results demonstrated that calpain mediates excitotoxic signals through mobilization of proapoptotic factors in a caspase-independent manner. These mutant mice will serve as useful tools for investigating calpain involvement in various diseases.
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Cites
Molecular characterization of mitochondrial apoptosis-inducing factor
Susin, S. A., Lorenzo, H. K., Zamzami, N., Marzo, I., Snow, B. E., Brothers, G. M., Mangion, J., Jacotot, E., Costantini, P., Loeffler, M., et al. (1999) · Nature · doi:10.1038/17135 · Cited by 4,060
Memantine in Moderate-to-Severe Alzheimer's Disease
Reisberg, B., Doody, R., Stöffler, A., Schmitt, F., Ferris, S., & Möbius, H. J. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa013128 · Cited by 2,043
Endonuclease G is an apoptotic DNase when released from mitochondria
Li, L. Y., Luo, X., & Wang, X. (2001) · Nature · doi:10.1038/35083620 · Cited by 1,787
Gomi, H., Yokoyama, T., Fujimoto, K., Ikeda, T., Katoh, A., Itoh, T., & Itohara, S. (1995) · Neuron · doi:10.1016/0896-6273(95)90238-4 · Cited by 256
Self-citation
Cited by
Single App knock-in mouse models of Alzheimer’s disease
Saito, T., Matsuba, Y., Mihira, N., Takano, J., Nilsson, P., Itohara, S., Iwata, N., & Saido, T. C. (2014) · Nature Neuroscience · doi:10.1038/nn.3697 · Cited by 1,366
Self-citationFricker, M., Tolkovsky, A. M., Borutaite, V., Coleman, M., & Brown, G. C. (2018) · Physiological Reviews · doi:10.1152/physrev.00011.2017 · Cited by 1,108
Cell death by necrosis: towards a molecular definition
Golstein, P., & Kroemer, G. (2007) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2006.11.001 · Cited by 1,044
APP mouse models for Alzheimer’s disease preclinical studies.
Sasaguri, H., Nilsson, P., Hashimoto, S., Nagata, K., Saito, T., De Strooper, B., Hardy, J., Vassar, R., Winblad, B., & Saido, T. C. (2017) · The EMBO Journal · doi:10.15252/embj.201797397 · Cited by 793
Self-citationCaspase-independent cell death
Kroemer, G., & Martin, S. J. (2005) · Nature Medicine · doi:10.1038/nm1263 · Cited by 716
Metadata
- Authors
- Takano, J., Tomioka, M., Tsubuki, S., Higuchi, M., Iwata, N., Itohara, S., Maki, M., & Saido, T. C.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2005-04
- Volume
- 280
- Issue
- 16
- Pages
- 16175-16184
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2009272717
- Cited by
- 180
- References
- 4
- FWCI
- 6.93
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Takano, J., Tomioka, M., Tsubuki, S., Higuchi, M., Iwata, N., Itohara, S., Maki, M., & Saido, T. C. (2005). Calpain Mediates Excitotoxic DNA Fragmentation via Mitochondrial Pathways in Adult Brains. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m414552200
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
