ArticleBrain research2012
Presenilin-null cells have altered two-pore calcium channel expression and lysosomal calcium: implications for lysosomal function.
Article in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Lysosome repair fails in ageing and Alzheimer's disease.Nature cell biology · 2025Article
- Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.Nature cell biology · 2025Article
- Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases.npj metabolic health and disease · 2025Review
- Effect of applied cadence in repeated sprint cycling on muscle characteristics.European journal of applied physiology · 2024Article
- C. elegans Presenilin Mediates Inter-Organelle Contacts and Communication that Is Required for Lysosome Activity.Aging and disease · 2024Article
- Genome-wide structural variant analysis identifies risk loci for non-Alzheimer's dementias.Cell genomics · 2023Article
- NAADP-induced intracellular calcium ion is mediated by the TPCs (two-pore channels) in hypoxia-induced pulmonary arterial hypertension.Journal of cellular and molecular medicine · 2021Article
- CaCells · 2020Review
- Mitophagy regulates integrity of mitochondria at synapses and is critical for synaptic maintenance.EMBO reports · 2020Article
- The Interplay between CaInternational journal of molecular sciences · 2019Review
- Review
- Endolysosomal CaFrontiers in cell and developmental biology · 2019Review
- Altered γ-Secretase Processing of APP Disrupts Lysosome and Autophagosome Function in Monogenic Alzheimer's Disease.Cell reports · 2018Article
- Two-pore channels and disease.Biochimica et biophysica acta. Molecular cell research · 2018Review
- Presenilins as Drug Targets for Alzheimer's Disease-Recent Insights from Cell Biology and Electrophysiology as Novel Opportunities in Drug Development.International journal of molecular sciences · 2018Review
- The role of CaDisease models & mechanisms · 2017Review
- Article
- Two-pore channels (TPCs): Novel voltage-gated ion channels with pleiotropic functions.Channels (Austin, Tex.) · 2017Review
- Endolysosomal two-pore channels regulate autophagy in cardiomyocytes.The Journal of physiology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Presenilins are necessary for calcium homeostasis and also for efficient proteolysis through the autophagy/lysosome system. Presenilin regulates both endoplasmic reticulum calcium stores and autophagic proteolysis in a γ-secretase independent fashion. The endo-lysosome system can also act as a calcium store, with calcium efflux channels being recently identified as two-pore channels 1 and 2. Here we investigated lysosomal calcium content and the channels that mediate calcium release from these acidic stores in presenilin knockout cells. We report that presenilin loss leads to a lower total lysosomal calcium store despite the buildup of lysosomes found in these cells. Additionally, we find alterations in two-pore calcium channel protein expression, with loss of presenilin preventing the formation of a high molecular weight species of TPC1 and TPC2. Finally, we find that treatments that disturb lysosomal calcium release lead to a reduction in autophagy function yet lysosomal inhibitors do not alter two-pore calcium channel expression. These data indicate that alterations in lysosomal calcium in the absence of presenilins might be leading to disruptions in autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.