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Development of ATP13A2-deficient In vitro Model for PARK9 Parkinson’s Disease
Conclusion: ATP13A2-deficient PD model was successfully developed.
Source: Current Signal Transduction Therapy - November 3, 2021 Category: Molecular Biology Source Type: research

Bioinformatics analyses show dysregulation of calcium-related genes in Angelman syndrome mouse model.
Abstract BACKGROUND: Angelman syndrome (AS) is a genetic neurodevelopmental disorder caused by the loss of function of the UBE3A protein in the brain. In a previous study, we showed that activity-dependent calcium dynamics in hippocampal CA1 pyramidal neurons of AS mice is compromised, and its normalization rescues the hippocampal-dependent deficits. Therefore, we expected that the expression profiles of calcium-related genes would be altered in AS mice hippocampi. METHODS: We analyzed mRNA sequencing data from AS model mice and WT controls in light of the newly published CaGeDB database of calcium-related ge...
Source: Neurobiology of Disease - November 16, 2020 Category: Neurology Authors: Panov J, Kaphzan H Tags: Neurobiol Dis Source Type: research

Nitrendipine, an antihypertensive alpha calcium channel blocker, is cytotoxic to neuroblastoma cells
ConclusionNTD induced apoptosis on neuroblastoma cells, appears to be independent of the expression of the L-type calcium channel.
Source: Molecular and Cellular Toxicology - September 30, 2019 Category: Cytology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Silencing the ACAT1 Gene in Human SH-SY5Y Neuroblastoma Cells Inhibits the Expression of Cyclo-Oxygenase 2 (COX2) and Reduces β-Amyloid-Induced Toxicity Due to Activation of Protein Kinase C (PKC) and ERK.
CONCLUSIONS Silencing ACAT1 attenuates Aβ₂₅₋₃₅-induced cytotoxicity and cell apoptosis in SH-SY5Y cells, which may due to the synergistic effect of ACAT1 and COX2 through PKC/ERK pathways. PMID: 30541014 [PubMed - in process]
Source: Medical Science Monitor - December 14, 2018 Category: Research Tags: Med Sci Monit Source Type: research

Tocopherol suppresses 24(S)-hydroxycholesterol-induced cell death via inhibition of CaMKII phosphorylation.
Abstract Although 24(S)-hydroxycholesterol (24S-OHC) plays an important role to maintain homeostasis of cholesterol in the brain, it induces neuronal cell death at high concentrations. 24S-OHC-induced cell death was suppressed by γ-tocopherol (γ-Toc) but not by γ-tocotrienol (γ-Toc3) in a similar way to α-tocopherol (α-Toc) and α-tocotrienol (α-Toc3) in human neuroblastoma SH-SY5Y cells. Both γ-Toc and γ-Toc3 significantly inhibited cumene hydroperoxide-induced cell death, as previously shown in the case of α-Toc and α-Toc3. Lipid droplet-like structure formation induced by 24S-OHC was suppressed by ne...
Source: Biochimie - September 26, 2018 Category: Biochemistry Authors: Kimura Y, Asa M, Urano Y, Saito Y, Nishikawa K, Noguchi N Tags: Biochimie Source Type: research

Amlodipine prevents apoptotic cell death by correction of elevated intracellular calcium in a primary neuronal model of Batten disease (CLN3 disease).
Abstract CLN3 disease (Spielmeyer-Vogt-Sjogren-Batten disease) is a severe pediatric neurodegenerative disorder for which there is currently no effective treatment. The disease is characterized by progressive neuronal death, which may be triggered by abnormal intracellular calcium levels leading to neuronal apoptosis. Previously, we demonstrated reversal of the calcium effect in a neuroblastoma cell line using amlodipine and other calcium channel antagonists. In the present studies, we developed a CLN3 siRNA-inhibited primary rat neuron model to further study etoposide-induced calcium changes and apoptosis in CLN3...
Source: Biochemical and Biophysical Research communications - June 12, 2013 Category: Biochemistry Authors: Warnock A, Tan L, Li C, Haack KA, Narayan SB, Bennett MJ Tags: Biochem Biophys Res Commun Source Type: research