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

Normal brain development in PS1 hypomorphic mice with markedly reduced gamma-secretase cleavage of betaAPP.

Neurobiology of aging - 1 Jan 2000

Rozmahel R, Huang J, Chen F, Liang Y, Nguyen V, Ikeda M, Levesque G, Yu G, Nishimura M, Mathews P, Schmidt S D, Mercken M, Bergeron C, Westaway D, St George-Hyslop P

Abstract excerpt

Presenilin 1-null mice die at birth from brain and skeletal developmental deformities due to disrupted Notch signaling. Presenilin 1-null mice also have severely reduced gamma-secretase cleavage of betaAPP. The assumption has been that facilitation of Notch signaling and betaAPP processing by presenilin 1 are analogous functions. Here we describe a presenilin 1-targetted mouse model that expresses extremely low...

Read the complete abstract on PubMed

Topics

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

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

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Antibody Specificity

Share to Aspartic Acid Endopeptidases

Share to Endopeptidases

Share to Gene Targeting

Share to Presenilin-1

Share to Spinal Cord

Source

Identifiers

PMID: 11804702
DOI: 10.1016/s0197-4580(01)00267-6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Normal brain development in PS1 hypomorphic mice with markedly reduced gamma-secretase cleavage of betaAPP.PMID 11804702Read ↗

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

Skeletal and CNS defects in Presenilin-1-deficient mice.Semantic proximity Read ↗

Role of presenilin in gamma-secretase cleavage of amyloid precursor protein.Semantic proximity Read ↗

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

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.Semantic proximity Read ↗

APH-1a Is the Principal Mammalian APH-1 Isoform Present in γ-Secretase Complexes during Embryonic DevelopmentSemantic 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 ↗

An Alzheimer's disease-linked PS1 variant rescues the developmental abnormalities of PS1-deficient embryos.Semantic proximity Read ↗

Generation and Characterization of a Novel Knockin Mouse Model Expressing PSEN1 D385A: Implications for Investigating Herbal Drug Effects in γ-Secretase Activity.Semantic proximity Read ↗

A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activity.Semantic proximity Read ↗

Insensitivity to Abeta42-lowering nonsteroidal anti-inflammatory drugs and gamma-secretase inhibitors is common among aggressive presenilin-1 mutations.Semantic proximity Read ↗

Human Presenilin-1 delivered by AAV9 rescues impaired γ-secretase activity, memory deficits, and neurodegeneration in Psen mutant mice.Semantic proximity Read ↗

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