ArticleThe Journal of cell biology1997
Increased apoptosis arising from increased expression of the Alzheimer's disease-associated presenilin-2 mutation (N141I).
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 119 citations in OpenAlex.
- Alzheimer's disease PSEN-2 N141I mutation reveals altered and shear-sensitive brain endothelial cell-like phenotype in human iPSC-derived models.Acta neuropathologica communications · 2025Article
- The Nuclear Lamina: Protein Accumulation and Disease.Biomedicines · 2020Review
- Overexpression of human Atp13a2Isoform-1 protein protects cells against manganese and starvation-induced toxicity.PloS one · 2019Article
- Inhibition of the Neuronal Calcium Sensor DREAM Modulates Presenilin-2 Endoproteolysis.Frontiers in molecular neuroscience · 2018Article
- Overexpression of N141I PS2 increases γ-secretase activity through up-regulation of Presenilin and Pen-2 in brain mitochondria of NSE/hPS2m transgenic mice.Laboratory animal research · 2016Article
- Exercise and early-onset Alzheimer's disease: theoretical considerations.Dementia and geriatric cognitive disorders extra · 2012Article
- Constitutive cAMP response element binding protein (CREB) activation by Alzheimer's disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Ubiquilin functions in autophagy and is degraded by chaperone-mediated autophagy.Human molecular genetics · 2010Article
- p53-dependent control of transactivation of the Pen2 promoter by presenilins.Journal of cell science · 2009Article
- Presenilin: RIP and beyond.Seminars in cell & developmental biology · 2009Review
- Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease.Neurochemistry international · 2009Review
- Dimerization of ubiquilin is dependent upon the central region of the protein: evidence that the monomer, but not the dimer, is involved in binding presenilins.The Biochemical journal · 2006Article
- Neuronal cell death in Alzheimer's disease and a neuroprotective factor, humanin.Current neuropharmacology · 2006Article
- Changes in presenilin 2-binding Wnt proteins, behavior, amyloid-beta 42, gamma-secretase activity, and testosterone sensitivity in transgenic mice coexpressing tetracycline-controlled transactivator and human mutant presenilin 2.Neuromolecular medicine · 2006Article
- Ubiquilin regulates presenilin endoproteolysis and modulates gamma-secretase components, Pen-2 and nicastrin.The Biochemical journal · 2005Article
- Differentially expressed genes in transgenic mice carrying human mutant presenilin-2 (N141I): correlation of selenoprotein M with Alzheimer's disease.Neurochemical research · 2005Article
- Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Adenovirus E3-6.7K maintains calcium homeostasis and prevents apoptosis and arachidonic acid release.Journal of virology · 2002Article
- Identification of ubiquilin, a novel presenilin interactor that increases presenilin protein accumulation.The Journal of cell biology · 2000Article
- Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the genes for presenilin 1 and 2 (PS-1 and PS-2) have been linked to development of early-onset Alzheimer's disease (AD). As neither the normal function of either presenilin is known nor why mutations cause disease, we examined the properties of wild-type, truncated, and mutant PS-2 upon expression in HeLa cells. Although HeLa cells are strongly predisposed to continued mitosis, expression of PS-2 induced programmed cell death (apoptosis). Direct evidence for apoptosis was obtained by double staining for terminal deoxynucleotide transferase nick end labeling (TUNEL) and PS-2 expression and by following green fluorescent protein-tagged PS-2 over time. Deletion analysis indicates that as little as 166 NH2-terminal residues of PS-2 are sufficient for endoplasmic reticulum (ER) localization and apoptosis. Moreover, the AD- associated PS-2 missense mutation (N141I) more efficiently induced cell death compared to wild-type PS-2 despite lower mutant protein accumulation. Expression of the presenilins in several other cell lines and transgenic mice has been accompanied by rapid protein cleavage without the induction of cell death. In contrast, PS-2 expressed in HeLa cells was not cleaved, and cell death occurred. We hypothesize that full-length but not cleaved PS-2 may be important in the regulation or induction of apoptosis.
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