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Amyloidogenic Mutations in Human Apolipoprotein A-I are not Necessarily Destabilizing: A Common Mechanism of ApoA-I Misfolding in Familial Amyloidosis and Atherosclerosis

High-density lipoproteins (HDLs) and their major protein, apoA-I, remove excess cellular cholesterol and protect against atherosclerosis. However, in acquired amyloidosis, non-variant full-length apoA-I deposits as fibrils in atherosclerotic plaques; in familial amyloidosis, N-terminal fragments of...

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Autores principales: Das, Madhurima, Mei, Xiaohu, Jayaraman, Shobini, Atkinson, David, Gursky, Olga
Formato: Artigo
Lenguaje:Inglês
Publicado: 2014
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Acceso en línea:https://ncbi.nlm.nih.gov/pmc/articles/PMC4047191/
https://ncbi.nlm.nih.gov/pubmed/24702826
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/febs.12809
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