The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
GM1-Ganglioside Accumulation at the Mitochondria-Associated ER Membranes Links ER Stress to Ca2+-Dependent Mitochondrial Apoptosis
Open accessAbstract
Summary Mitochondria-associated ER membranes or MAMs define the sites of endoplasmic reticulum/mitochondria juxtaposition that control Ca2+ flux between these organelles. We found that in a mouse model of the human lysosomal storage disease GM1-gangliosidosis, GM1-ganglioside accumulates in the glycosphingolipid-enriched microdomain (GEM) fractions of MAMs, where it interacts with the phosphorylated form of IP3 receptor-1, influencing the activity of this channel. Ca2+ depleted from the ER is then taken up by the mitochondria, leading to Ca2+ overload in this organelle. The latter induces mitochondrial membrane permeabilization (MMP), opening of the permeability transition pore and activation of the mitochondrial apoptotic pathway. This study identifies the GEMs as the sites of Ca2+ diffusion between the ER and the mitochondria. We propose a new mechanism of Ca2+-mediated apoptotic signalling, whereby GM1 accumulation at the GEMs alters Ca2+ dynamics and acts as a molecular effector of both ER stress–induced and mitochondria-mediated apoptosis of neuronal cells.
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Cites
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“Lastly, we measured ROS production, which increases with excessive [Ca]m (Emerit et al., 2004), by labeling MEFs with 20,70dichlorofluorescein, a specific ROS indicator.”
MethodMitochondrial membrane permeabilization in cell death
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Mitofusin 2 tethers endoplasmic reticulum to mitochondria
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BAX and BAK Regulation of Endoplasmic Reticulum Ca 2+ : A Control Point for Apoptosis
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Self-citationMitochondrial dynamics and apoptosis
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“GM1 Accumulation in the GEMs Alters Mitochondrial Ca Homeostasis We first observed overt changes in mitochondrial shape, a phenomenon consequential to disturbance of mitochondrial Ca concentration ([Ca]m) (Suen et al., 2008).”
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Cited by
Platt, F. M., d’Azzo, A., Davidson, B. L., Neufeld, E. F., & Tifft, C. J. (2018) · Nature Reviews Disease Primers · doi:10.1038/s41572-018-0025-4 · Cited by 1,052
Self-citationOxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives
Hajam, Y. A., Rani, R., Ganie, S. Y., Sheikh, T. A., Javaid, D., Qadri, S. S., Pramodh, S., Alsulimani, A., Alkhanani, M. F., Harakeh, S., et al. (2022) · Cells · doi:10.3390/cells11030552 · Cited by 915
Lysosomal storage disorders: The cellular impact of lysosomal dysfunction
Platt, F. M., Boland, B., & van der Spoel, A. C. (2012) · Journal of Cell Biology · doi:10.1083/jcb.201208152 · Cited by 689
Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases
Hetz, C., & Mollereau, B. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3689 · Cited by 684
Upregulated function of mitochondria‐associated ER membranes in Alzheimer disease
Area‐Gomez, E., del Carmen Lara Castillo, M., Tambini, M. D., Guardia‐Laguarta, C., de Groof, A. J. C., Madra, M., Ikenouchi, J., Umeda, M., Bird, T. D., Sturley, S. L., et al. (2012) · The EMBO Journal · doi:10.1038/emboj.2012.202 · Cited by 638
Metadata
- Authors
- Sano, R., Annunziata, I., Patterson, A., Moshiach, S., Gomero, E., Opferman, J., Forte, M., & d'Azzo, A.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 36
- Issue
- 3
- Pages
- 500-511
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2053599433
- Cited by
- 288
- References
- 51
- FWCI
- 11.81
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Sano, R., Annunziata, I., Patterson, A., Moshiach, S., Gomero, E., Opferman, J., Forte, M., & d'Azzo, A. (2009). GM1-Ganglioside Accumulation at the Mitochondria-Associated ER Membranes Links ER Stress to Ca2+-Dependent Mitochondrial Apoptosis. Molecular Cell. https://doi.org/10.1016/j.molcel.2009.10.021
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