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

Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function.

Proceedings of the National Academy of Sciences of the United States of America - 17 Mar 1998

Guo Q, Christakos S, Robinson N, Mattson M P

Abstract excerpt

Mutations in the presenilin 1 (PS-1) gene account for many cases of early-onset autosomal dominant inherited forms of Alzheimer's disease. Recent findings suggest that PS-1 mutations may sensitize neurons to apoptosis induced by trophic factor withdrawal and exposure to amyloid beta-peptide (Abet...

Read the complete abstract on PubMed

Topics

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

Share to Apoptosis
Share to Calcium
Share to Membrane Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitochondria

Share to Mutation

Share to Nerve Tissue Proteins

Share to Recombinant Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 9501245
DOI: 10.1073/pnas.95.6.3227
PMCID: PMC19724

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-9501245-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function.PMID 9501245Read ↗

Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid beta-peptide: involvement of calcium and oxyradicals.Semantic proximity Read ↗

Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 is linked to perturbed calcium homeostasis and enhanced oxyradical production.Semantic proximity Read ↗

Secreted beta-amyloid precursor protein counteracts the proapoptotic action of mutant presenilin-1 by activation of NF-kappaB and stabilization of calcium homeostasis.Semantic proximity Read ↗

Alzheimer's PS-1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid beta-peptide.Semantic proximity Read ↗

Increased vulnerability of hippocampal neurons from presenilin-1 mutant knock-in mice to amyloid beta-peptide toxicity: central roles of superoxide production and caspase activation.Semantic proximity Read ↗

Presenilin-1 mutations sensitize neurons to DNA damage-induced death by a mechanism involving perturbed calcium homeostasis and activation of calpains and caspase-12.Semantic proximity Read ↗

Presenilin-1 mutation alters NGF-induced neurite outgrowth, calcium homeostasis, and transcription factor (AP-1) activation in PC12 cells.Semantic proximity Read ↗

Presenilin-1-deficient neurons are nitric oxide-dependently killed by hydrogen peroxide in vitro.Semantic proximity Read ↗

Alzheimer's disease-like alterations in peripheral cells from presenilin-1 transgenic mice.Semantic proximity Read ↗

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

Cholinergic-like neurons carrying PSEN1 E280A mutation from familial Alzheimer’s disease reveal intraneuronal Aβ42 peptide accumulation, hyperphosphorylation of TAU, oxidative stress, apoptosis and Ca2+ flux dysregulation: Therapeutic ImplicationsSemantic proximity Read ↗

Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice.Semantic proximity Read ↗

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