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

Notch-1 activation by familial Alzheimer's disease (FAD)-linked mutant forms of presenilin-1.

Journal of neuroscience research - 15 Oct 2000

Nakajima M, Shimizu T, Shirasawa T

Abstract excerpt

We prepared a cleavage site-directed antibody against Notch-1, that specifically recognized the cleaved Notch-1 intracellular domain (NICD). To assess Notch-1 processing and its nuclear localization in familial Alzheimer's disease (FAD)-linked presenilin-1 (PS-1) mutants, we overexpressed wild type, M146V, A246E, C410Y, or deltaE9 PS-1 mutant with a membrane-bound Notch-1 in a PS-1-deficient cell line. On Western...

Read the complete abstract on PubMed

Topics

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

Share to 3T3 Cells
Share to Alzheimer Disease
Share to Presenilin-1

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Rabbits

Share to Receptor, Notch1

Share to Receptors, Cell Surface

Share to Transfection

Share to Translocation, Genetic

Source

Identifiers

PMID: 11020224
DOI: 10.1002/1097-4547(20001015)62:2<311::AID-JNR16>3.0.CO;2-G

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Notch-1 activation by familial Alzheimer's disease (FAD)-linked mutant forms of presenilin-1.PMID 11020224Read ↗

Proteolytic release and nuclear translocation of Notch-1 are induced by presenilin-1 and impaired by pathogenic presenilin-1 mutations.Semantic proximity Read ↗

A presenilin-1 mutation causes Alzheimer disease without affecting Notch signaling.Semantic proximity Read ↗

Presenilin-1 D257A and D385A mutants fail to cleave Notch in their endoproteolyzed forms, but only presenilin-1 D385A mutant can restore its gamma-secretase activity with the compensatory overexpression of normal C-terminal fragment.Semantic proximity Read ↗

Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing.Semantic proximity Read ↗

Wild-type presenilin 1 protects against Alzheimer disease mutation-induced amyloid pathology.Semantic proximity Read ↗

Familial Alzheimer's disease-associated mutations block translocation of full-length presenilin 1 to the nuclear envelope.Semantic proximity Read ↗

Cell surface presenilin-1 participates in the gamma-secretase-like proteolysis of Notch.Semantic proximity Read ↗

Presenilin-1 mutations reduce cytoskeletal association, deregulate neurite growth, and potentiate neuronal dystrophy and tau phosphorylation.Semantic proximity Read ↗

Nicastrin is dispensable for gamma-secretase protease activity in the presence of specific presenilin mutations.Semantic proximity Read ↗

Presenilins mediate a dual intramembranous gamma-secretase cleavage of Notch-1.Semantic proximity Read ↗

Secretion of the Notch-1 Abeta-like peptide during Notch signaling.Semantic proximity Read ↗

Inhibition of neurite outgrowth by familial Alzheimer's disease-linked presenilin-1 mutations.Semantic proximity Read ↗

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