Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Susceptibility to cellular stress in PS1 mutant N2a cells is associated with mitochondrial defects and altered calcium homeostasis.

Scientific reports - 15 Apr 2020

Rojas-Charry Liliana, Calero-Martinez Sergio, Morganti Claudia, Morciano Giampaolo, Park Kyungeun, Hagel Christian, Marciniak Stefan J, Glatzel Markus, Pinton Paolo, Sepulveda-Falla Diego

Abstract excerpt

Presenilin 1 (PS1) mutations are the most common cause of familial Alzheimer's disease (FAD). PS1 also plays a role in cellular processes such as calcium homeostasis and autophagy. We hypothesized that mutant presenilins increase cellular vulnerability to stress. We stably expressed human PS1, mutant PS1E280A and mutant PS1Δ9 in mouse neuroblastoma N2a cells. We examined early signs of stress in different...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyloid beta-Peptides
Share to Amyloid Precursor Protein Secretases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Autophagy

Share to Calcium

Share to Endoplasmic Reticulum

Share to Oxidative Stress

Share to Peptide Fragments

Share to Presenilin-1

Source

Open in PubMed Open full text

Identifiers

PMID: 32296078
DOI: 10.1038/s41598-020-63254-7
PMCID: PMC7160112

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Susceptibility to cellular stress in PS1 mutant N2a cells is associated with mitochondrial defects and altered calcium homeostasis.PMID 32296078Read ↗

Presenilin 1 Regulates Membrane Homeostatic Pathways that are Dysregulated in Alzheimer’s DiseaseSemantic proximity Read ↗

Alzheimer's disease-causing presenilin-1 mutations have deleterious effects on mitochondrial function.Semantic proximity Read ↗

PSEN2 (presenilin 2) mutants linked to familial Alzheimer disease impair autophagy by altering Ca2+ homeostasisSemantic proximity Read ↗

Presenilin 1 (PS1) located at mitochondrial inner membrane regulates mitochondrial cristae junction proteins arrangement and cristae formation in HEK293 cellsSemantic proximity Read ↗

Neurons overexpressing mutant presenilin-1 are more sensitive to apoptosis induced by endoplasmic reticulum-Golgi stress.Semantic proximity Read ↗

Familial Alzheimer disease–linked mutations specifically disrupt Ca2+ leak function of presenilin 1Semantic proximity Read ↗

Impaired mitochondrial function due to familial Alzheimer's disease-causing presenilins mutants via Ca2+ disruptionsSemantic proximity Read ↗

Familial Alzheimer's disease mutations in presenilins: effects on endoplasmic reticulum calcium homeostasis and correlation with clinical phenotypes.Semantic proximity Read ↗

Presenilin-deficient neurons and astrocytes display normal mitochondrial phenotypesSemantic proximity Read ↗

Presenilin 2 modulates endoplasmic reticulum (ER)-mitochondria interactions and Ca2+ cross-talk.Semantic proximity Read ↗

Cellular consequences of the expression of Alzheimer's disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cells.Semantic proximity Read ↗

Degradative organelles containing mislocalized alpha-and beta-synuclein proliferate in presenilin-1 null neurons.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.