The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Role of SERCA1 Truncated Isoform in the Proapoptotic Calcium Transfer from ER to Mitochondria during ER Stress
Open accessAbstract
SUMMARY Among the new players at the endoplasmic reticulum (ER)-mitochondria interface regulating interorganelle calcium signaling, those specifically involved during ER stress are not known at present. We report here that the truncated variant of the sarcoendoplasmic reticulum Ca2+-ATPase 1 (S1T) amplifies ER stress through the PERK-eIF2α-ATF4-CHOP pathway. S1T, which is localized in the ER-mitochondria microdomains, determines ER Ca2+ depletion due to increased Ca2+ leak, an increased number of ER-mitochondria contact sites, and inhibition of mitochondria movements. This leads to increased Ca2+ transfer to mitochondria in both resting and stimulated conditions and activation of the mitochondrial apoptotic pathway. Interestingly, S1T knockdown was shown to prevent ER stress, mitochondrial Ca2+ overload, and subsequent apoptosis. Thus, by bridging ER stress to apoptosis through increased ER-mitochondria Ca2+ transfer, S1T acts as an essential determinant of cellular fate.
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Cites
The versatility and universality of calcium signalling
Berridge, M. J., Lipp, P., & Bootman, M. D. (2000) · Nature Reviews Molecular Cell Biology · doi:10.1038/35036035 · Cited by 5,701
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Mediators of endoplasmic reticulum stress-induced apoptosis
Szegezdi, E., Logue, S. E., Gorman, A. M., & Samali, A. (2006) · The EMBO Reports · doi:10.1038/sj.embor.7400779 · Cited by 2,345
Brostrom, M. A., & Brostrom, C. O. (2003) · Cell Calcium · doi:10.1016/s0143-4160(03)00127-1 · Cited by 197
Cited by
Zhao, L., Zhang, H., Li, N., Chen, J., Xu, H., Wang, Y., & Liang, Q. (2023) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2023.116306 · Cited by 963
PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress
Verfaillie, T., Rubio, N., Garg, A. D., Bultynck, G., Rizzuto, R., Decuypere, J.-P., Piette, J., Linehan, C., Gupta, S., Samali, A., et al. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2012.74 · Cited by 850
Self-citationMfn2 modulates the UPR and mitochondrial function via repression of PERK
Muñoz, J. P., Ivanova, S., Sánchez‐Wandelmer, J., Martínez‐Cristóbal, P., Noguera, E., Sancho, A., Díaz‐Ramos, A., Hernández‐Alvarez, M. I., Sebastián, D., Mauvezin, C., et al. (2013) · The EMBO Journal · doi:10.1038/emboj.2013.168 · Cited by 451
Organization and Function of Membrane Contact Sites
Helle, S. C. J., Kanfer, G., Kolar, K., Lang, A., Michel, A. H., & Kornmann, B. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2013.01.028 · Cited by 453
New functions of mitochondria associated membranes in cellular signaling
van Vliet, A. R., Verfaillie, T., & Agostinis, P. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2014.03.009 · Cited by 353
Metadata
- Authors
- Chami, M., Oulès, B., Szabadkai, G., Tacine, R., Rizzuto, R., & Paterlini-Bréchot, P.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 32
- Issue
- 5
- Pages
- 641-651
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2112195082
- Cited by
- 239
- References
- 4
- FWCI
- 4.86
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Chami, M., Oulès, B., Szabadkai, G., Tacine, R., Rizzuto, R., & Paterlini-Bréchot, P. (2008). Role of SERCA1 Truncated Isoform in the Proapoptotic Calcium Transfer from ER to Mitochondria during ER Stress. Molecular Cell. https://doi.org/10.1016/j.molcel.2008.11.014
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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