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

Generation and initial characterization of FDD knock in mice.

PloS one - 18 Nov 2009

Giliberto Luca, Matsuda Shuji, Vidal Ruben, D'Adamio Luciano

Abstract excerpt

BACKGROUND: Mutations in the integral membrane protein 2B, also known as BRI(2), a type II trans-membrane domain protein cause two autosomal dominant neurodegenerative diseases, Familial British and Danish Dementia. In these conditions, accumulation of a C-terminal peptide (ABri and ADan) cleaved off from the mutated precursor protein by the pro-protein convertase furin, leads to amyloid deposition in the walls...

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 Brain
Share to Dementia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Primers

Share to Mice, Transgenic

Share to Neurodegenerative Diseases

Share to Peptides

Share to Protein Structure, Tertiary

Source

Open in PubMed Open full text

Identifiers

PMID: 19924302
DOI: 10.1371/journal.pone.0007900
PMCID: PMC2774945

Genes

APP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Generation and initial characterization of FDD knock in mice.PMID 19924302Read ↗

Memory Deficits Due to Familial British Dementia<i>BRI2</i>Mutation Are Caused by Loss of<i>BRI2</i>Function Rather than AmyloidosisSemantic proximity Read ↗

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits.Semantic proximity Read ↗

Cerebral amyloid angiopathy and parenchymal amyloid deposition in transgenic mice expressing the Danish mutant form of human BRI2.Semantic proximity Read ↗

APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.Semantic proximity Read ↗

Danish and British dementia ITM2b/BRI2 mutations reduce BRI2 protein stability and impair glutamatergic synaptic transmission.Semantic proximity Read ↗

BRI2 as a central protein involved in neurodegeneration.Semantic proximity Read ↗

Familial Danish dementia young Knock-in rats expressing humanized APP and human Aβ show impaired pre and postsynaptic glutamatergic transmissionSemantic proximity Read ↗

A decamer duplication in the 3′ region of the <i>BRI</i> gene originates an amyloid peptide that is associated with dementia in a Danish kindredSemantic proximity Read ↗

The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production.Semantic proximity Read ↗

Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.Semantic proximity Read ↗

Proteolytic processing of familial British dementia-associated BRI variants: evidence for enhanced intracellular accumulation of amyloidogenic peptides.Semantic proximity Read ↗

Increased tau phosphorylation and tau truncation, and decreased synaptophysin levels in mutant BRI2/tau transgenic mice.Semantic proximity Read ↗

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