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Article

Evidence for early cytotoxic aggregates in transgenic mice for human transthyretin Leu55Pro.

The American journal of pathology - 1 Nov 2002

Sousa Mónica Mendes, Fernandes Rui, Palha Joana Almeida, Taboada Ana, Vieira Paulo, Saraiva Maria João

Abstract excerpt

Familial amyloidotic polyneuropathy (FAP) is a lethal autosomal dominant disorder characterized by systemic extracellular deposition of transthyretin (TTR) amyloid fibrils. Several groups have generated transgenic mice carrying human TTR Val30Met, the most common mutation in FAP. To study amyloidogenicity and cytotoxicity of different TTRs, we produced transgenic mice expressing human TTR Leu55Pro, one of the...

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Source

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Identifiers

PMID: 12414539
DOI: 10.1016/S0002-9440(10)64469-0
PMCID: PMC1850789

Genes

TTR
FAP

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

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Research trail→

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Evidence for early cytotoxic aggregates in transgenic mice for human transthyretin Leu55Pro.PMID 12414539Read ↗

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Cysteine 10 is a key residue in amyloidogenesis of human transthyretin Val30Met.Semantic proximity Read ↗

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Tissue damage in the amyloidoses: Transthyretin monomers and nonnative oligomers are the major cytotoxic species in tissue culture.Semantic proximity Read ↗

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