CALHM1 and its polymorphism P86L differentially control Ca2+ homeostasis, mitogen‐activated protein kinase signaling, and cell vulnerability upon exposure to amyloid β

Summary The mutated form of the Ca2+ channel CALHM1 (Ca2+ homeostasis modulator 1), P86L‐CALHM1, has been correlated with early onset of Alzheimer's disease (AD). P86L‐CALHM1 increases production of amyloid beta (Aβ) upon extracellular Ca2+ removal and its subsequent addback. The aim of this st...

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Veröffentlicht in:	Aging cell 2015-12, Vol.14 (6), p.1094-1102
Hauptverfasser:	Moreno‐Ortega, Ana José, Buendia, Izaskun, Mouhid, Lamia, Egea, Javier, Lucea, Susana, Ruiz‐Nuño, Ana, López, Manuela G., Cano‐Abad, María F.
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - genetics Alzheimer's disease Amyloid beta-Peptides - metabolism Amyloid beta-protein Antibodies - immunology Apoptosis - physiology Ca2+ channel CALHM1 Ca2+ homeostasis Calcium - metabolism Calcium Channels - genetics Calcium Channels - immunology Calcium Channels - metabolism Caspase 3 - metabolism Caspase 7 - metabolism caspases Cell death Cell Line, Tumor Cell Survival - genetics CREB Cyclic AMP Response Element-Binding Protein - metabolism early apoptosis Extracellular Signal-Regulated MAP Kinases - metabolism Genetic aspects HeLa Cells Homeostasis Humans Ion Transport - genetics MAP Kinase Signaling System - genetics Membrane Glycoproteins - genetics Membrane Glycoproteins - immunology Membrane Glycoproteins - metabolism Mitogens Neurons Original Polymorphism, Single Nucleotide - genetics Protein kinases
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