ArticleScientific reports2017
Knockdown of amyloid precursor protein increases calcium levels in the endoplasmic reticulum.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Therapeutic potential of human microglia transplantation in a chimeric model of CSF1R-related leukoencephalopathy.Neuron · 2024Article
- Knockdown of Amyloid Precursor Protein Increases Ion Channel Expression and Alters CaInternational journal of molecular sciences · 2023Article
- Review
- APPsα rescues impaired CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Transgenic Mice Overexpressing HumanInternational journal of molecular sciences · 2020Article
- ALS-Associated SOD1(G93A) Decreases SERCA Pump Levels and Increases Store-Operated CaInternational journal of molecular sciences · 2019Article
- STIM Proteins and Glutamate Receptors in Neurons: Role in Neuronal Physiology and Neurodegenerative Diseases.International journal of molecular sciences · 2019Review
- Putative autoantibodies in the cerebrospinal fluid of Alzheimer's disease patients.F1000Research · 2019Article
- Role of STIM1 in neurodegeneration.World journal of biological chemistry · 2018Review
- STIM1 deficiency is linked to Alzheimer's disease and triggers cell death in SH-SY5Y cells by upregulation of L-type voltage-operated CaJournal of molecular medicine (Berlin, Germany) · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial Alzheimer's disease (AD) is caused by mutations in the genes that encode amyloid precursor protein (APP) and presenilins. Disturbances in calcium homeostasis have been observed in various cellular and animal models of AD and are proposed to underlie the pathogenesis of the disease. Furthermore, wildtype presenilins were shown to regulate endoplasmic reticulum (ER) calcium homeostasis, although their precise mechanism of action remains controversial. To investigate whether APP also affects ER calcium levels, we used RNA interference to target the APP gene in cultured T84 cells in combination with two types of ER calcium sensors. Using a genetically encoded calcium indicator, GEM-CEPIA1er, we found that APP-deficient cells exhibited elevated resting calcium levels in the ER and prolonged emptying of ER calcium stores upon the cyclopiazonic acid-induced inhibition of sarco-endoplasmic reticulum calcium-ATPase. These effects could be ascribed to lower ER calcium leakage rates. Consistent with these results, translocation of the endogenous ER calcium sensor STIM1 to its target channel Orai1 was delayed following ER calcium store depletion. Our data suggest a physiological function of APP in the regulation of ER calcium levels.
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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.