| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| P Westermark, K Sletten, B Johansson, G G Cornwel. Fibril in senile systemic amyloidosis is derived from normal transthyretin. Proceedings of the National Academy of Sciences of the United States of America. vol 87. issue 7. 1990-05-04. PMID:2320592. |
the amyloid fibril in senile systemic amyloidosis (ssa), like that of familial amyloidotic polyneuropathy, is derived from transthyretin (ttr). |
1990-05-04 |
2023-08-11 |
Not clear |
| P Westermark, K Sletten, B Johansson, G G Cornwel. Fibril in senile systemic amyloidosis is derived from normal transthyretin. Proceedings of the National Academy of Sciences of the United States of America. vol 87. issue 7. 1990-05-04. PMID:2320592. |
in familial amyloidotic polyneuropathy, the amyloidogenesis has been considered to depend on point mutations leading to ttr variants. |
1990-05-04 |
2023-08-11 |
Not clear |
| Y Sakaki, H Sasaki, K Yoshioka, H Furuy. Genetic analysis of familial amyloidotic polyneuropathy, an autosomal dominant disease. Clinica chimica acta; international journal of clinical chemistry. vol 185. issue 3. 1990-03-29. PMID:2559819. |
familial amyloidotic polyneuropathy (fap) is an autosomal dominant genetic disease, and the major component of the amyloid fibrils from fap patients was shown to be variants of transthyretin (ttr) with single amino acid substitutions. |
1990-03-29 |
2023-08-11 |
Not clear |
| K Shimada, S Maeda, T Murakami, S Nishiguchi, F Tashiro, S Yi, S Wakasugi, K Takahashi, K Yamamur. Transgenic mouse model of familial amyloidotic polyneuropathy. Molecular biology & medicine. vol 6. issue 4. 1990-03-20. PMID:2560117. |
familial amyloidotic polyneuropathy (fap) is a dominantly inherited disorder, characterized by the extracellular deposition of amyloid fibrils composed of variant transthyretin (ttr), and by prominent peripheral nerve involvement. |
1990-03-20 |
2023-08-11 |
mouse |
| Y Sakaki, K Yoshioka, H Tanahashi, H Furuya, H Sasak. Human transthyretin (prealbumin) gene and molecular genetics of familial amyloidotic polyneuropathy. Molecular biology & medicine. vol 6. issue 2. 1990-03-09. PMID:2693890. |
the variant types of ttr are known to be closely associated with familial amyloidotic polyneuropathy (fap), an autosomal dominant genetic disorder. |
1990-03-09 |
2023-08-11 |
mouse |
| H Furuya, M Nakazato, M J Saraiva, S P Costa, H Sasaki, H Matsuo, I Goto, Y Sakak. Tetramer formation of a variant type human transthyretin (prealbumin) produced by Escherichia coli expression system. Biochemical and biophysical research communications. vol 163. issue 2. 1989-10-20. PMID:2675831. |
a variant of human transthyretin(ttr, prealbumin) with methionine for valine substitution at position 30 is a major component of amyloid fibrils found in patients of familial amyloidotic polyneuropathy(fap) type i, an autosomal dominant genetic disease. |
1989-10-20 |
2023-08-11 |
human |
| M J Saraiva, I L Alves, P P Cost. Simplified method for screening populations at risk for transthyretin Met30-associated familial amyloidotic polyneuropathy. Clinical chemistry. vol 35. issue 6. 1989-07-21. PMID:2543515. |
this simple, reliable method for detecting the transthyretin-methionine30 [ttr(met30)] mutation, found in patients with familial amyloidotic polyneuropathy (fap), is based on production of an extra peptide fragment when the mutant ttr is treated with cyanogen bromide (cnbr). |
1989-07-21 |
2023-08-11 |
Not clear |
| I J Holt, A E Harding, L Middleton, G Chrysostomou, G Said, R H King, P K Thoma. Molecular genetics of amyloid neuropathy in Europe. Lancet (London, England). vol 1. issue 8637. 1989-04-14. PMID:2564060. |
the portuguese type of familial amyloid polyneuropathy (fap type i), a disabling autosomal dominant disorder with onset in early adult life, is caused by a point mutation in the transthyretin (ttr; previously known as prealbumin) gene. |
1989-04-14 |
2023-08-11 |
Not clear |
| M J Saraiva, P P Costa, M do R Almeida, A Banzhoff, K Altland, A Ferlini, G Rubboli, R Plasmati, C A Tassinari, G Rome. Familial amyloidotic polyneuropathy: transthyretin (prealbumin) variants in kindreds of Italian origin. Human genetics. vol 80. issue 4. 1989-01-18. PMID:2848756. |
as part of an epidemiological study that aims to characterize chemically the mutation(s) in transthyretin (ttr) related to familial amyloidotic polyneuropathy (fap) of different ethnic origins, studies were carried out on ttr from two fap kindreds of italian origin. |
1989-01-18 |
2023-08-11 |
Not clear |
| M Tanaka, S Hirai, E Matsubara, K Okamoto, M Morimatsu, M Nakazat. Familial amyloidotic polyneuropathy without familial occurrence: carrier detection by the radioimmunoassay of variant transthyretin. Journal of neurology, neurosurgery, and psychiatry. vol 51. issue 4. 1988-07-15. PMID:3379433. |
in order to establish the diagnosis of non-hereditary primary amyloidotic polyneuropathy, it must be confirmed that variant ttr is absent in the serum of relatives. |
1988-07-15 |
2023-08-11 |
Not clear |
| R L Martone, J Herbert, A Dwork, E A Scho. Transthyretin is synthesized in the mammalian eye. Biochemical and biophysical research communications. vol 151. issue 2. 1988-04-14. PMID:3279959. |
the finding of ttr synthesis in the eye may explain ocular involvement in the familial amyloidotic polyneuropathies. |
1988-04-14 |
2023-08-11 |
rat |
| A Ferlini, G Romeo, C A Tassinari, M J Saraiva, P P Costa, F Salv. Discrimination of peripheral polyneuropathies caused by TTR variant or diabetes in the same pedigree through protein studies. Advances in neurology. vol 48. 1988-01-20. PMID:3334782. |
discrimination of peripheral polyneuropathies caused by ttr variant or diabetes in the same pedigree through protein studies. |
1988-01-20 |
2023-08-11 |
Not clear |
| M J Saraiva, P P Costa, D S Goodma. Genetic expression of a transthyretin mutation in typical and late-onset Portuguese families with familial amyloidotic polyneuropathy. Neurology. vol 36. issue 11. 1986-11-21. PMID:3762958. |
two studies were conducted to explore questions concerning the expression of a mutant transthyretin (ttr) gene, found in portuguese patients with familial amyloidotic polyneuropathy (fap). |
1986-11-21 |
2023-08-11 |
Not clear |
| H Sasaki, S Tone, M Nakazato, K Yoshioka, H Matsuo, Y Kato, Y Sakak. Generation of transgenic mice producing a human transthyretin variant: a possible mouse model for familial amyloidotic polyneuropathy. Biochemical and biophysical research communications. vol 139. issue 2. 1986-10-31. PMID:3021142. |
type i familial amyloidotic polyneuropathy (fap) results from the systemic deposition of a plasma transthyretin (ttr) variant with a val----met change at position 30. |
1986-10-31 |
2023-08-11 |
mouse |
| M J Saraiva, W Sherman, D S Goodma. Presence of a plasma transthyretin (prealbumin) variant in familial amyloidotic polyneuropathy in a kindred of Greek origin. The Journal of laboratory and clinical medicine. vol 108. issue 1. 1986-07-24. PMID:3011930. |
human plasma transthyretin (ttr, a protein formerly called prealbumin) is known to be associated with familial amyloidotic polyneuropathy (fap) of autosomal inheritance. |
1986-07-24 |
2023-08-11 |
human |
| M Nakazato, T Kurihara, S Matsukura, K Kangawa, H Matsu. Diagnostic radioimmunoassay for familial amyloidotic polyneuropathy before clinical onset. The Journal of clinical investigation. vol 77. issue 5. 1986-06-03. PMID:3457802. |
the purpose of this study is to develop an early diagnostic method for familial amyloidotic polyneuropathy (fap) before clinical manifestations appear around the age of 30 yr. amyloid fibrils isolated from type i fap (fap1) of portuguese, swedish, and japanese origins consist of a variant transthyretin (ttr) that contains a methionine-for-valine substitution at position 30 or a mixture of normal ttr and this variant form. |
1986-06-03 |
2023-08-11 |
Not clear |
| M J Saraiva, P P Costa, D S Goodma. Biochemical marker in familial amyloidotic polyneuropathy, Portuguese type. Family studies on the transthyretin (prealbumin)-methionine-30 variant. The Journal of clinical investigation. vol 76. issue 6. 1986-02-06. PMID:3908483. |
a transthyretin variant with a methionine for valine substitution at position 30 [ttr(met30)] is found in portuguese patients with familial amyloidotic polyneuropathy (fap). |
1986-02-06 |
2023-08-11 |
human |
| M J Saraiva, S Birken, P P Costa, D S Goodma. Family studies of the genetic abnormality in transthyretin (prealbumin) in Portuguese patients with familial amyloidotic polyneuropathy. Annals of the New York Academy of Sciences. vol 435. 1985-05-13. PMID:6099706. |
studies were conducted on ttr isolated from sera of patients with familial amyloidotic polyneuropathy (fap), and on amyloid fibril protein (afp) isolated from tissues of two portuguese patients who died with fap. |
1985-05-13 |
2023-08-12 |
human |
| M J Saraiva, S Birken, P P Costa, D S Goodma. Amyloid fibril protein in familial amyloidotic polyneuropathy, Portuguese type. Definition of molecular abnormality in transthyretin (prealbumin). The Journal of clinical investigation. vol 74. issue 1. 1984-07-31. PMID:6736244. |
amyloid fibril protein in patients with familial amyloidotic polyneuropathy is known to be chemically related to transthyretin (ttr), the plasma protein that is usually referred to as prealbumin. |
1984-07-31 |
2023-08-12 |
Not clear |
| M J Saraiva, P P Costa, D S Goodma. Studies on plasma transthyretin (prealbumin) in familial amyloidotic polyneuropathy, Portuguese type. The Journal of laboratory and clinical medicine. vol 102. issue 4. 1983-11-23. PMID:6311926. |
studies were conducted to investigate whether or not portuguese patients with familial amyloidotic polyneuropathy (fap) have an abnormal species of ttr circulating in their plasma and, if so, whether this might have any impact on vitamin a transport and retinol-binding protein (rbp) metabolism in these patients. |
1983-11-23 |
2023-08-12 |
human |