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Highly expressed in choroid plexus epithelial cells. Detected in retina pigment epithelium and liver"}],"commentType":"TISSUE SPECIFICITY"},{"texts":[{"value":"Each monomer has two 4-stranded beta sheets and the shape of a prolate ellipsoid. Antiparallel beta-sheet interactions link monomers into dimers. A short loop from each monomer forms the main dimer-dimer interaction. These two pairs of loops separate the opposed, convex beta-sheets of the dimers to form an internal channel"}],"commentType":"DOMAIN"},{"texts":[{"evidences":[{"evidenceCode":"ECO:0000269","source":"PubMed","id":"14760718"},{"evidenceCode":"ECO:0000269","source":"PubMed","id":"16335952"},{"evidenceCode":"ECO:0000269","source":"PubMed","id":"19167329"}],"value":"Not glycosylated under normal conditions. Following unfolding, caused for example by variant AMYLD1 'Gly-38', the cryptic Asn-118 site is exposed and glycosylated by STT3B-containing OST complex, leading to its degradation by the ER-associated degradation (ERAD) pathway"}],"commentType":"PTM"},{"texts":[{"evidences":[{"evidenceCode":"ECO:0000305","source":"PubMed","id":"17175208"}],"value":"Sulfonation of the reactive cysteine Cys-30 enhances the stability of the native conformation of TTR, avoiding misassembly of the protein leading to amyloid formation"}],"commentType":"PTM"},{"commentType":"DISEASE","disease":{"diseaseId":"Amyloidosis, hereditary systemic 1","diseaseAccession":"DI-00100","acronym":"AMYLD1","description":"A form of hereditary systemic amyloidosis, a disorder characterized by amyloid deposition in multiple tissues resulting in a wide clinical spectrum. AMYLD1 is an autosomal dominant form due to transthyretin amyloid deposition. Protein fibrils can form in different tissues leading to amyloid polyneuropathies, amyloidotic cardiomyopathy, carpal tunnel syndrome, systemic senile amyloidosis. The disease includes leptomeningeal amyloidosis that is characterized by primary involvement of the central nervous system. Neuropathologic examination shows amyloid in the walls of leptomeningeal vessels, in pia arachnoid, and subpial deposits. Some patients also develop vitreous amyloid deposition that leads to visual impairment (oculoleptomeningeal amyloidosis). Clinical features include seizures, stroke-like episodes, dementia, psychomotor deterioration, variable amyloid deposition in the vitreous 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