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The Presenilin-2 Loop Peptide Perturbs Intracellular Ca2+ Homeostasis and Accelerates Apoptosis
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
inferredcites →https://doi.org/10.1006/meth.2001.1186openalex-snapshot
TAT-Mediated Protein Transduction into Mammalian Cells
inferredcites →https://doi.org/10.1016/0014-5793(96)00608-4openalex-snapshot
Characterization of human presenilin 1 using N‐terminal specific monoclonal antibodies: Evidence that Alzheimer mutations affect proteolytic processing
inferredcites →https://doi.org/10.1016/s0006-3495(00)76441-1openalex-snapshot
A Direct Optimization Approach to Hidden Markov Modeling for Single Channel Kinetics
inferredcites →https://doi.org/10.1016/s0014-5793(96)01142-8openalex-snapshot
Alzheimer‐associated presenilin‐2 confers increased sensitivity to poptosis in PC12 cells
inferredcites →https://doi.org/10.1016/s0014-5793(99)00108-8openalex-snapshot
Identification of caspases that cleave presenilin‐1 and presenilin‐2
inferredcites →https://doi.org/10.1016/s0896-6273(00)00066-0openalex-snapshot
Presenilin-Mediated Modulation of Capacitative Calcium Entry
inferredcites →https://doi.org/10.1016/s0925-4439(00)00028-4openalex-snapshot
Presenilin structure, function and role in Alzheimer disease
inferredcites →https://doi.org/10.1016/s0962-8924(00)01771-2openalex-snapshot
Protein transduction: unrestricted delivery into all cells?
inferredcites →https://doi.org/10.1038/34910openalex-snapshot
Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein
inferredcites →https://doi.org/10.1038/375754a0openalex-snapshot
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
inferredcites →https://doi.org/10.1038/376775a0openalex-snapshot
Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene
inferredcites →https://doi.org/10.1038/4042openalex-snapshot
Transduction of full-length TAT fusion proteins into mammalian cells: TAT-p27Kip1 induces cell migration
inferredcites →https://doi.org/10.1038/4710openalex-snapshot
Killing HIV-infected cells by transduction with an HIV protease-activated caspase-3 protein
inferredcites →https://doi.org/10.1038/ncb1063openalex-snapshot
Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis
inferredcites →https://doi.org/10.1038/ncb1302openalex-snapshot
The endoplasmic reticulum gateway to apoptosis by Bcl-XL modulation of the InsP3R
inferredcites →https://doi.org/10.1038/ncb788openalex-snapshot
Dysfunction of store-operated calcium channel in muscle cells lacking mg29
inferredcites →https://doi.org/10.1038/sj.cr.7290281openalex-snapshot
Overexpression of Bax sensitizes prostate cancer cells to TGF-β induced apoptosis
inferredcites →https://doi.org/10.1046/j.1471-4159.2001.00638.xopenalex-snapshot
Pro‐apoptotic effect of presenilin 2 (PS2) overexpression is associated with down‐regulation of Bcl‐2 in cultured neurons
inferredcites →https://doi.org/10.1073/pnas.0408352102openalex-snapshot
Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum
inferredcites →https://doi.org/10.1073/pnas.062059899openalex-snapshot
Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons
inferredcites →https://doi.org/10.1073/pnas.95.26.15821openalex-snapshot
Inositol 1,4,5-tris-phosphate activation of inositol tris-phosphate receptor Ca 2+ channel by ligand tuning of Ca 2+ inhibition
inferredcites →https://doi.org/10.1073/pnas.96.4.1391openalex-snapshot
Phosphorylation of presenilin-2 regulates its cleavage by caspases and retards progression of apoptosis
inferredcites →https://doi.org/10.1074/jbc.271.49.31025openalex-snapshot
Requirement of the Familial Alzheimer's Disease Gene PS2 for Apoptosis
inferredcites →https://doi.org/10.1074/jbc.272.17.11006openalex-snapshot
Endoproteolytic Cleavage and Proteasomal Degradation of Presenilin 2 in Transfected Cells
inferredcites →https://doi.org/10.1074/jbc.272.45.28415openalex-snapshot
Evidence That Levels of Presenilins (PS1 and PS2) Are Coordinately Regulated by Competition for Limiting Cellular Factors
inferredcites →https://doi.org/10.1074/jbc.273.51.33909openalex-snapshot
Abrogation of the Presenilin 1/β-Catenin Interaction and Preservation of the Heterodimeric Presenilin 1 Complex following Caspase Activation
inferredcites →https://doi.org/10.1074/jbc.275.5.3173openalex-snapshot
The Transmembrane Aspartates in Presenilin 1 and 2 Are Obligatory for γ-Secretase Activity and Amyloid β-Protein Generation
inferredcites →https://doi.org/10.1074/jbc.m104986200openalex-snapshot
Unreliability of the Cytochromec-Enhanced Green Fluorescent Fusion Protein as a Marker of Cytochrome c Release in Cells That Overexpress Bcl-2
inferredcites →https://doi.org/10.1074/jbc.m212379200openalex-snapshot
The C-terminal Fragment of Presenilin 2 Triggers p53-mediated Staurosporine-induced Apoptosis, a Function Independent of the Presenilinase-derived N-terminal Counterpart
inferredcites →https://doi.org/10.1074/jbc.m908329199openalex-snapshot
Depletion of Intracellular Ca2+ by Caffeine and Ryanodine Induces Apoptosis of Chinese Hamster Ovary Cells Transfected with Ryanodine Receptor
inferredcites →https://doi.org/10.1083/jcb.139.2.485openalex-snapshot
Increased Apoptosis Arising from Increased Expression of the Alzheimer's Disease–associated Presenilin-2 Mutation (N141I)
inferredcites →https://doi.org/10.1083/jcb.149.4.793openalex-snapshot
Capacitative Calcium Entry Deficits and Elevated Luminal Calcium Content in Mutant Presenilin-1 Knockin Mice
inferredcites →https://doi.org/10.1085/jgp.109.5.571openalex-snapshot
Single-Channel Kinetics, Inactivation, and Spatial Distribution of Inositol Trisphosphate (IP3) Receptors in Xenopus Oocyte Nucleus
inferredcites →https://doi.org/10.1096/fj.05-4198comopenalex-snapshot
Inhibition of mechanosensitive cation channels inhibits myogenic differentiation by suppressing the expression of myogenic regulatory factors and caspase‐3 activity
inferredcites →https://doi.org/10.1126/science.271.5248.521openalex-snapshot
Interfering with Apoptosis: Ca 2+ -Binding Protein ALG-2 and Alzheimer's Disease Gene ALG-3
inferredcites →https://doi.org/10.1126/science.274.5287.521openalex-snapshot
Book Reviews Science and Dissent in Post-Mao China, reviewed by M. Goldman * Comparative Vertebrate Neuroanatomy, E. G. Jones * Particle Physics, P. Forman * Vignette * Browsings
inferredcites →https://doi.org/10.1126/science.274.5293.1710openalex-snapshot
Participation of Presenilin 2 in Apoptosis: Enhanced Basal Activity Conferred by an Alzheimer Mutation
inferredcites →https://doi.org/10.1126/science.277.5324.373openalex-snapshot
Alternative Cleavage of Alzheimer-Associated Presenilins During Apoptosis by a Caspase-3 Family Protease
inferredcites →https://doi.org/10.1126/science.285.5433.1569openalex-snapshot
In Vivo Protein Transduction: Delivery of a Biologically Active Protein into the Mouse
inferredcites →https://doi.org/10.1158/0008-5472.can-05-0395openalex-snapshot
A Bifunctional Targeted Peptide that Blocks HER-2 Tyrosine Kinase and Disables Mitochondrial Function in HER-2-Positive Carcinoma Cells
inferredcites →https://doi.org/10.1242/jcs.114.12.2223openalex-snapshot
Mechanisms of capacitative calcium entry
inferredcites →https://doi.org/10.1523/jneurosci.17-11-04212.1997openalex-snapshot
Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid beta-peptide: involvement of calcium and oxyradicals.
inferredcites →https://doi.org/10.1523/jneurosci.18-23-09790.1998openalex-snapshot
Overexpression in Neurons of Human Presenilin-1 or a Presenilin-1 Familial Alzheimer Disease Mutant Does Not Enhance Apoptosis
inferredcites →https://doi.org/10.1523/jneurosci.4386-03.2004openalex-snapshot
Dysregulated IP3Signaling in Cortical Neurons of Knock-In Mice Expressing an Alzheimer's-Linked Mutation inPresenilin1Results in Exaggerated Ca2+Signals and Altered Membrane Excitability
What points at this work
Incoming claims: where this work appears in other papers’ reference lists and arguments.
inferred← citeshttps://doi.org/10.2139/ssrn.3952082openalex-extracted
Neuronal Loss of NCLX-Dependent Mitochondrial Calcium Efflux Contributes to Age-Associated Cognitive Decline
inferred← citeshttps://doi.org/10.1002/9781118185537.ch4openalex-snapshot
Multitarget Drugs for Stabilization of Calcium Cycling and Neuroprotection in Neurodegenerative Diseases and Stroke
inferred← citeshttps://doi.org/10.1007/978-3-642-40282-1_28openalex-snapshot
IP3 Receptors in Neurodegenerative Disorders: Spinocerebellar Ataxias and Huntington’s and Alzheimer’s Diseases
inferred← citeshttps://doi.org/10.1007/s00018-009-8435-9openalex-snapshot
Presenilin-dependent regulated intramembrane proteolysis and γ-secretase activity
inferred← citeshttps://doi.org/10.1007/s00018-011-0845-9openalex-snapshot
Intracellular organelles in the saga of Ca2+ homeostasis: different molecules for different purposes?
inferred← citeshttps://doi.org/10.1007/s10495-007-0719-7openalex-snapshot
IP3 receptors in cell survival and apoptosis: Ca2+ release and beyond
inferred← citeshttps://doi.org/10.1007/s11064-009-0054-1openalex-snapshot
BACE and γ-Secretase Characterization and Their Sorting as Therapeutic Targets to Reduce Amyloidogenesis
inferred← citeshttps://doi.org/10.1016/b978-0-12-814513-5.00009-xopenalex-snapshot
Epigenome-Wide DNA Methylation and Histone Modification of Alzheimer's Disease
inferred← citeshttps://doi.org/10.1016/b978-0-323-99209-1.00010-7openalex-snapshot
Familial cerebral amyloid disorders with prominent white matter involvement
inferred← citeshttps://doi.org/10.1016/j.bbamcr.2014.03.007openalex-snapshot
Inositol 1,4,5-trisphosphate receptor-isoform diversity in cell death and survival
inferred← citeshttps://doi.org/10.1016/j.bbamcr.2014.05.011openalex-snapshot
At the right distance: ER-mitochondria juxtaposition in cell life and death
inferred← citeshttps://doi.org/10.1016/j.bbrc.2016.09.053openalex-snapshot
Dysregulation of neuronal calcium homeostasis in Alzheimer's disease – A therapeutic opportunity?
inferred← citeshttps://doi.org/10.1016/j.brainresbull.2009.07.007openalex-snapshot
Caspase substrates and neurodegenerative diseases
inferred← citeshttps://doi.org/10.1016/j.ceca.2008.03.004openalex-snapshot
The N-terminus of presenilin-2 increases single channel activity of brain ryanodine receptors through direct protein–protein interaction
inferred← citeshttps://doi.org/10.1016/j.ceca.2017.06.008openalex-snapshot
Calcium signaling and molecular mechanisms underlying neurodegenerative diseases
inferred← citeshttps://doi.org/10.1016/j.cellsig.2010.07.018openalex-snapshot
Pannexin channels in ATP release and beyond: An unexpected rendezvous at the endoplasmic reticulum
inferred← citeshttps://doi.org/10.1016/j.isci.2023.106296openalex-snapshot
Neuronal loss of NCLX-dependent mitochondrial calcium efflux mediates age-associated cognitive decline
inferred← citeshttps://doi.org/10.1016/j.molmed.2009.01.001openalex-snapshot
Calcium signaling and neurodegenerative diseases
inferred← citeshttps://doi.org/10.1016/j.nbd.2007.05.002openalex-snapshot
Analysis of alteration of p75NTR processing and signalling by PS2 mutation and γ-secretase inhibition
inferred← citeshttps://doi.org/10.1016/j.neuint.2007.06.020openalex-snapshot
Neurosecretases provide strategies to treat sporadic and familial Alzheimer disorders
inferred← citeshttps://doi.org/10.1016/j.plipres.2012.07.001openalex-snapshot
Sphingolipids: Critical players in Alzheimer’s disease
inferred← citeshttps://doi.org/10.1016/j.procbio.2017.09.012openalex-snapshot
Expression, purification, and preliminary characterization of human presenilin-2
inferred← citeshttps://doi.org/10.1016/j.resp.2007.11.005openalex-snapshot
Contrast between cardiac left ventricle and diaphragm muscle in expression of genes involved in carbohydrate and lipid metabolism
inferred← citeshttps://doi.org/10.1016/j.tins.2008.06.005openalex-snapshot
Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease
inferred← citeshttps://doi.org/10.1016/j.tins.2012.06.004openalex-snapshot
Caspase-3 in the central nervous system: beyond apoptosis
inferred← citeshttps://doi.org/10.1021/cn3001069openalex-snapshot
Stabilizers of Neuronal and Mitochondrial Calcium Cycling as a Strategy for Developing a Medicine for Alzheimer's Disease
inferred← citeshttps://doi.org/10.1074/jbc.m114.629584openalex-snapshot
Presenilin-like GxGD Membrane Proteases Have Dual Roles as Proteolytic Enzymes and Ion Channels
inferred← citeshttps://doi.org/10.1074/jbc.m115.682385openalex-snapshot
High Glucose-induced Retinal Pericyte Apoptosis Depends on Association of GAPDH and Siah1
inferred← citeshttps://doi.org/10.1074/jbc.m710601200openalex-snapshot
Glucose and Endoplasmic Reticulum Calcium Channels Regulate HIF-1β via Presenilin in Pancreatic β-Cells
inferred← citeshttps://doi.org/10.1089/ars.2009.2788openalex-snapshot
Potential Therapeutic Benefits of Strategies Directed to Mitochondria
inferred← citeshttps://doi.org/10.1101/cshperspect.a041758openalex-snapshot
Calcium Signaling and Pathogenesis of Neurodegenerative Disorders: Potential Therapeutic Opportunities
inferred← citeshttps://doi.org/10.1111/j.1346-8138.2008.00513.xopenalex-snapshot
Interleukin‐18 prevents apoptosis via PI3K/Akt pathway in normal human keratinocytes
inferred← citeshttps://doi.org/10.1111/j.1582-4934.2010.01208.xopenalex-snapshot
γ‐secretase complexes containing caspase‐cleaved presenilin‐1 increase intracellular Aβ42/Aβ40 ratio
inferred← citeshttps://doi.org/10.1152/ajpendo.00191.2007openalex-snapshot
Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart
inferred← citeshttps://doi.org/10.1177/1535370213514317openalex-snapshot
Thapsigargin affects presenilin-2 but not presenilin-1 regulation in SK-N-BE cells
inferred← citeshttps://doi.org/10.1212/01.wnl.0000310643.53587.87openalex-snapshot
A novel PSEN2 mutation associated with a peculiar phenotype
inferred← citeshttps://doi.org/10.1371/annotation/f8cecc73-06ec-4bba-b07a-a3bc2a08f4c7openalex-snapshot
Correction: Intracellular Calcium Deficits in Drosophila Cholinergic Neurons Expressing Wild Type or FAD-Mutant Presenilin
inferred← citeshttps://doi.org/10.1371/journal.pone.0006904openalex-snapshot
Intracellular Calcium Deficits in Drosophila Cholinergic Neurons Expressing Wild Type or FAD-Mutant Presenilin
inferred← citeshttps://doi.org/10.1523/jneurosci.1554-10.2010openalex-snapshot
Role of Presenilins in Neuronal Calcium Homeostasis
inferred← citeshttps://doi.org/10.3233/jad-2010-100306openalex-snapshot
Neuronal Calcium Signaling, Mitochondrial Dysfunction, and Alzheimer's Disease
inferred← citeshttps://doi.org/10.32607/20758251-2010-2-1-72-80openalex-snapshot
Calcium Signaling and Neurodegeneration
inferred← citeshttps://doi.org/10.3389/fphar.2012.00061openalex-snapshot
Physiology and Pathology of Calcium Signaling in the Brain
inferred← citeshttps://doi.org/10.35376/10324/16193openalex-snapshot
Remodelado del calcio intracelular y susceptibilidad a la muerte neuronal en el envejecimiento y en la enfermedad de Alzheimer
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