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

Cortical dysplasia resembling human type 2 lissencephaly in mice lacking all three APP family members.

The EMBO journal - 13 Oct 2004

Herms Jochen, Anliker Brigitte, Heber Sabine, Ring Sabine, Fuhrmann Martin, Kretzschmar Hans, Sisodia Sangram, Müller Ulrike

Abstract excerpt

The Alzheimer's disease beta-amyloid precursor protein (APP) is a member of a larger gene family that includes the amyloid precursor-like proteins, termed APLP1 and APLP2. We previously documented that APLP2-/-APLP1-/- and APLP2-/-APP-/- mice die postnatally, while APLP1-/-APP-/- mice and single mutants were viable. We now report that mice lacking all three APP/APLP family members survive through embryonic...

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 Animals, Newborn

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

Share to Cerebral Cortex

Share to Crosses, Genetic

Share to Embryonic Development

Share to Immunohistochemistry

Share to Survival Rate

Source

Open in PubMed Open full text

Identifiers

PMID: 15385965
DOI: 10.1038/sj.emboj.7600390
PMCID: PMC524337

Genes

APP
APLP1
APLP2

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

Cortical dysplasia resembling human type 2 lissencephaly in mice lacking all three APP family members.PMID 15385965Read ↗

Mice with combined gene knock-outs reveal essential and partially redundant functions of amyloid precursor protein family members.Semantic proximity Read ↗

Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenotype.Semantic proximity Read ↗

Redundancy and divergence in the amyloid precursor protein family.Semantic proximity Read ↗

Neurons Generated from APP/APLP1/APLP2 Triple Knockout Embryonic Stem Cells Behave Normally in Vitro and in Vivo: Lack of Evidence for a Cell Autonomous Role of the Amyloid Precursor Protein in Neuronal DifferentiationSemantic proximity Read ↗

Generation of conditional null alleles for APP and APLP2.Semantic proximity Read ↗

The function of presenilin-1 in amyloid beta-peptide generation and brain development.Semantic proximity Read ↗

Functions of the APP gene family in the nervous system: insights from mouse modelsSemantic proximity Read ↗

Regulation of gene expression by the APP family in the adult cerebral cortexSemantic proximity Read ↗

Truncating mutations in APP cause a distinct neurological phenotype.Semantic proximity Read ↗

Cellular functions of the amyloid precursor protein from development to dementia.Semantic proximity Read ↗

Amyloid precursor protein mediates deficits in corticogenesis in Down syndrome cortical organoidsSemantic proximity Read ↗

β2 and γ3 laminins are critical cortical basement membrane components: Ablation of Lamb2 and Lamc3 genes disrupts cortical lamination and produces dysplasiaSemantic proximity Read ↗

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