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

Identification of loci determining susceptibility to the lethal effects of amyloid precursor protein transgene overexpression.

Human molecular genetics - 15 Sept 2004

Krezowski Joseph, Knudson Danielle, Ebeling Christine, Pitstick Rose, Giri Ranjit K, Schenk Dale, Westaway David, Younkin Linda, Younkin Steven G, Ashe Karen Hsiao, Carlson George A

Abstract excerpt

Phenotypes produced by expression of human amyloid precursor protein (APP) transgenes vary depending on the genetic background of the mouse. FVB/N mice overexpressing human APP695 develop a central nervous system disorder and die prematurely, precluding development of Abeta peptide amyloid plaques. 129S6 mice are resistant to the lethal effects of APP overexpression, allowing sufficient levels of Abeta expression...

Read the complete abstract on PubMed

Topics

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

Share to Alzheimer Disease
Share to Amyloid beta-Peptides

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

Share to Amyloid beta-Protein Precursor

Share to Chromosome Mapping

Share to Genes, Lethal

Share to Mice, Mutant Strains

Share to Peptide Fragments

Share to Transgenes

Source

Identifiers

PMID: 15254013
DOI: 10.1093/hmg/ddh210

Genes

APP

Variants

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identification of loci determining susceptibility to the lethal effects of amyloid precursor protein transgene overexpression.PMID 15254013Read ↗

Genetic modification of the phenotypes produced by amyloid precursor protein overexpression in transgenic mice.Semantic proximity Read ↗

Mapping genetic modulators of amyloid plaque deposition in TgCRND8 transgenic mice.Semantic proximity Read ↗

Alzheimer's disease: molecular genetics and transgenic animal models.Semantic proximity Read ↗

Effect of the Icelandic Mutation APPA673T in the Murine APP Gene on Phenotype of Line 66 Tau Mice.Semantic proximity Read ↗

Enhanced amyloidogenic processing of the beta-amyloid precursor protein in gene-targeted mice bearing the Swedish familial Alzheimer's disease mutations and a "humanized" Abeta sequence.Semantic proximity Read ↗

The effect of the Icelandic mutation APP <sup>A673T</sup> in the line 66 model of tauopathySemantic proximity Read ↗

Mice expressing the Swedish APP mutation on a 129 genetic background demonstrate consistent behavioral deficits and pathological markers of Alzheimer's disease.Semantic proximity Read ↗

Mutations associated with a locus for familial Alzheimer's disease result in alternative processing of amyloid beta-protein precursor.Semantic proximity Read ↗

Increased susceptibility to ischemic brain damage in transgenic mice overexpressing the amyloid precursor protein.Semantic proximity Read ↗

Mice Deficient for the Amyloid Precursor Protein GeneSemantic proximity Read ↗

Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice.Semantic proximity Read ↗

A transgenic rat model of Alzheimer's disease with extracellular Abeta deposition.Semantic proximity Read ↗

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