ArticleBiochemistry and biophysics reports2016
Genetic background modifies amyloidosis in a mouse model of ATTR neuropathy.
Article in Biochemistry and biophysics reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Hereditary vitreoretinal amyloidosis with transthyretin Gly83Arg variant, a long-term study.Eye (London, England) · 2025Article
- Novel Therapeutic Application of Self-Assembly Peptides Targeting the Mitochondria inInternational journal of molecular sciences · 2020Article
- Increased Risk of Multiple Outpatient Surgeries in African-American Carriers ofJournal of clinical medicine · 2019Article
- Nanoparticle-Based Delivery of CRISPR/Cas9 Genome-Editing Therapeutics.The AAPS journal · 2018Review
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8 authors.
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Abstract
Penetrance and age of onset of ATTRV30M amyloidotic neuropathy varies significantly among different populations. This variability has been attributed to both genetic and environmental modifiers. We studied the effect of genetic background on phenotype in two lines of transgenic mice bearing the same ATTRV30M transgene. Amyloid deposition, transthyretin (TTR), megalin, clusterin and disease markers of endoplasmic reticulum stress, the ubiquitin-proteasome system, apoptosis, and complement activation were assessed with WB and immunohistochemistry in donor and recipient tissue. Our results indicate that genetic background modulates amyloid deposition by influencing TTR handling in recipient tissue and may partly account for the marked variability in penetrance observed in various world populations.
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