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Communicative & Integrative Biology Volume 4, 2011 - Issue 3

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Presenilin-2 modulation of ER-mitochondria interactions

FAD mutations, mechanisms and pathological consequences

Enrico Zampese Department of Biomedical Sciences, University of Padova and CNR Institute of Neuroscience; Padova, ItalCorrespondence[email protected]

Cristina Fasolato Department of Biomedical Sciences, University of Padova and CNR Institute of Neuroscience; Padova, Ital

Tullio Pozzan Department of Biomedical Sciences, University of Padova and CNR Institute of Neuroscience; Padova, Ital

Paola Pizzo Department of Biomedical Sciences, University of Padova and CNR Institute of Neuroscience; Padova, Ital

Pages 357-360 | Received 15 Feb 2011, Accepted 15 Feb 2011, Published online: 01 May 2011

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https://doi.org/10.4161/cib.4.3.15160

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Mark Makarov, Liliia Kushnireva, Michele Papa & Eduard Korkotian. (2023) Presenilins and mitochondria—an intriguing link: mini-review. Frontiers in Neuroscience 17.
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Robert E. Means & Samuel G. Katz. (2021) Balancing life and death: BCL‐2 family members at diverse ER–mitochondrial contact sites. The FEBS Journal 289:22, pages 7075-7112.
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Alice Rossi & Paola Pizzo. (2021) Mitochondrial bioenergetics and neurodegeneration: a paso doble. Neural Regeneration Research 16:4, pages 686.
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Elena Alberdi, Asier Ruiz, Maria Victoria Sánchez-Gómez, Estibaliz Capetillo-Zarate & Calos Matute. 2021. Mitochondrial Physiology and Vegetal Molecules. Mitochondrial Physiology and Vegetal Molecules 317 337 .

Marioly Müller, Ulises Ahumada-Castro, Mario Sanhueza, Christian Gonzalez-Billault, Felipe A. Court & César Cárdenas. (2018) Mitochondria and Calcium Regulation as Basis of Neurodegeneration Associated With Aging. Frontiers in Neuroscience 12.
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Maria Sol Herrera-Cruz & Thomas Simmen. (2017) Of yeast, mice and men: MAMs come in two flavors. Biology Direct 12:1.
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Ju Gao, Luwen Wang, Jingyi Liu, Fei Xie, Bo Su & Xinglong Wang. (2017) Abnormalities of Mitochondrial Dynamics in Neurodegenerative Diseases. Antioxidants 6:2, pages 25.
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Mario Agostini & Cristina Fasolato. (2016) When, where and how? Focus on neuronal calcium dysfunctions in Alzheimer’s Disease. Cell Calcium 60:5, pages 289-298.
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M Giacomello & L Pellegrini. (2016) The coming of age of the mitochondria–ER contact: a matter of thickness. Cell Death & Differentiation 23:9, pages 1417-1427.
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Luis Fernando Hernández-Zimbrón & Selva Rivas-Arancibia. (2016) Syntaxin 5 Overexpression and β -Amyloid 1–42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone Exposure . BioMed Research International 2016, pages 1-9.
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F Zeidán-Chuliá, B-HN de Oliveira, A B Salmina, M F Casanova, D P Gelain, M Noda, A Verkhratsky & J CF Moreira. (2014) Altered expression of Alzheimer’s disease-related genes in the cerebellum of autistic patients: a model for disrupted brain connectome and therapy. Cell Death & Disease 5:5, pages e1250-e1250.
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Tito CalìDenis OttoliniMarisa Brini. (2013) Calcium and Endoplasmic Reticulum-Mitochondria Tethering in Neurodegeneration. DNA and Cell Biology 32:4, pages 140-146.
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Arun Raturi & Thomas Simmen. (2013) Where the endoplasmic reticulum and the mitochondrion tie the knot: The mitochondria-associated membrane (MAM). Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1833:1, pages 213-224.
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Paola Pizzo, Ilaria Drago, Riccardo Filadi & Tullio Pozzan. (2012) Mitochondrial Ca2+ homeostasis: mechanism, role, and tissue specificities. Pfl?gers Archiv - European Journal of Physiology 464:1, pages 3-17.
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Enrico Zampese & Paola Pizzo. (2011) Intracellular organelles in the saga of Ca2+ homeostasis: different molecules for different purposes?. Cellular and Molecular Life Sciences 69:7, pages 1077-1104.
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Riccardo Filadi, Enrico Zampese, Tullio Pozzan, Paola Pizzo & Cristina Fasolato. 2012. Endoplasmic Reticulum Stress in Health and Disease. Endoplasmic Reticulum Stress in Health and Disease 75 106 .

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Presenilin-2 modulation of ER-mitochondria interactions

FAD mutations, mechanisms and pathological consequences

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Presenilin-2 modulation of ER-mitochondria interactions

FAD mutations, mechanisms and pathological consequences

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