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本文引用的文献
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Retention of misfolded mutant transthyretin by the chaperone BiP/GRP78 mitigates amyloidogenesis.
J Mol Biol. 2006 Feb 17;356(2):469-82. doi: 10.1016/j.jmb.2005.11.051. Epub 2005 Dec 5.
2
The biological and chemical basis for tissue-selective amyloid disease.
Cell. 2005 Apr 8;121(1):73-85. doi: 10.1016/j.cell.2005.01.018.
3
Tissue damage in the amyloidoses: Transthyretin monomers and nonnative oligomers are the major cytotoxic species in tissue culture.
Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2817-22. doi: 10.1073/pnas.0400062101. Epub 2004 Feb 23.
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Diflunisal analogues stabilize the native state of transthyretin. Potent inhibition of amyloidogenesis.
J Med Chem. 2004 Jan 15;47(2):355-74. doi: 10.1021/jm030347n.
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Therapeutic approaches to protein-misfolding diseases.
Nature. 2003 Dec 18;426(6968):905-9. doi: 10.1038/nature02265.
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Quality control in the endoplasmic reticulum protein factory.
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Tabulation of human transthyretin (TTR) variants, 2003.
Amyloid. 2003 Sep;10(3):160-84. doi: 10.3109/13506120308998998.
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Delta F508 CFTR pool in the endoplasmic reticulum is increased by calnexin overexpression.
Mol Biol Cell. 2004 Feb;15(2):563-74. doi: 10.1091/mbc.e03-06-0379. Epub 2003 Oct 31.
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