| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Bárbara Macedo, Ana Rita Batista, Nelson Ferreira, Maria Rosário Almeida, Maria João Saraiv. Anti-apoptotic treatment reduces transthyretin deposition in a transgenic mouse model of Familial Amyloidotic Polyneuropathy. Biochimica et biophysica acta. vol 1782. issue 9. 2008-10-15. PMID:18572024. |
since oxidative stress, apoptosis and inflammation are associated with transthyretin (ttr) deposition in familial amyloidotic polyneuropathy (fap), we investigated the possible tudca therapeutical application in this disease. |
2008-10-15 |
2023-08-12 |
mouse |
| Yukio Ando, Mitsuharu Ued. Novel methods for detecting amyloidogenic proteins in transthyretin related amyloidosis. Frontiers in bioscience : a journal and virtual library. vol 13. 2008-09-19. PMID:18508604. |
transthyretin (ttr)-related familial amyloidotic polyneuropathy (fap) is an autosomal dominant form of fatal hereditary amyloidosis. |
2008-09-19 |
2023-08-12 |
Not clear |
| C Zaros, E Genin, U Hellman, M A Saporta, L Languille, M Wadington-Cruz, O Suhr, M Misrahi, V Planté-Bordeneuv. On the origin of the transthyretin Val30Met familial amyloid polyneuropathy. Annals of human genetics. vol 72. issue Pt 4. 2008-09-05. PMID:18460047. |
transthyretin (ttr) familial amyloid polyneuropathy is a severe autosomal dominant neuropathy of adulthood, frequently linked to the pathogenic val30met variant of the ttr gene. |
2008-09-05 |
2023-08-12 |
Not clear |
| Tatsufumi Murakami, Yutaka Ohsawa, Yoshihide Sunad. The transthyretin gene is expressed in human and rodent dorsal root ganglia. Neuroscience letters. vol 436. issue 3. 2008-08-25. PMID:18406527. |
most cases of familial amyloidotic polyneuropathy (fap) are caused by ttr gene mutations, and characterized by amyloid deposition in the peripheral nervous system. |
2008-08-25 |
2023-08-12 |
mouse |
| Sofia Duque Santos, Joana Magalhães, Maria João Saraiv. Activation of the heat shock response in familial amyloidotic polyneuropathy. Journal of neuropathology and experimental neurology. vol 67. issue 5. 2008-06-20. PMID:18431252. |
here, we studied the heat shock response in familial amyloidotic polyneuropathy (fap), a neurodegenerative disease caused by aggregation and extracellular tissue deposition of mutated transthyretin (ttr). |
2008-06-20 |
2023-08-12 |
mouse |
| Luís Gales, Maria Rosário Almeida, Gemma Arsequell, Gregorio Valencia, Maria João Saraiva, Ana Margarida Dama. Iodination of salicylic acid improves its binding to transthyretin. Biochimica et biophysica acta. vol 1784. issue 3. 2008-05-15. PMID:18155178. |
transthyretin (ttr) is a plasma homotetrameric protein associated with senile systemic amyloidosis and familial amyloidotic polyneuropathy. |
2008-05-15 |
2023-08-12 |
Not clear |
| Yukio Ando, Hirofumi Jon. [Pathogenesis and therapy for transthyretin related amyloidosis]. Rinsho byori. The Japanese journal of clinical pathology. vol 56. issue 2. 2008-05-14. PMID:18402051. |
mutated forms of ttr are the precursor protein of familial amyloidotic polyneuropathy (fap). |
2008-05-14 |
2023-08-12 |
mouse |
| I Gonçalves, T Quintela, G Baltazar, M R Almeida, M J M Saraiva, C R Santo. Transthyretin interacts with metallothionein 2. Biochemistry. vol 47. issue 8. 2008-05-06. PMID:18237193. |
ttr is involved in two types of amyloid disease, the senile systemic amyloidosis and the familial amyloidotic polyneuropathy. |
2008-05-06 |
2023-08-12 |
human |
| Xu Hou, Adam Mechler, Lisandra L Martin, Marie-Isabel Aguilar, David H Smal. Cholesterol and anionic phospholipids increase the binding of amyloidogenic transthyretin to lipid membranes. Biochimica et biophysica acta. vol 1778. issue 1. 2008-03-20. PMID:18061140. |
deposition of transthyretin (ttr) amyloid is a pathological hallmark of familial amyloidotic polyneuropathy (fap). |
2008-03-20 |
2023-08-12 |
Not clear |
| Gösta Holmgren, Urban Hellman, Jenni Jonasson, Hans-Eric Lundgren, Per Westermark, Ole B Suh. A Swedish family with the rare Phe33Leu transthyretin mutation. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 12. issue 3. 2008-03-07. PMID:16194875. |
familial amyloidotic polyneuropathy (fap) designates ttr mutations where the phenotype is dominated by a peripheral sensory-motor polyneuropathy. |
2008-03-07 |
2023-08-12 |
Not clear |
| Takahiko Tokuda, Yo-Ichi Takei, Bunkichi Takayama, Yoshinobu Hoshii, Shu-Ichi Iked. Severe amyloid deposition in mammary glands of familial amyloid polyneuropathy patients. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 14. issue 3. 2008-02-19. PMID:17701472. |
clinical pictures of familial amyloid polyneuropathy (fap) vary considerably, perhaps because of the many gene mutations of transthyretin (ttr), but even in patients having the most common mutation of ttr (the substitution of methionine for valine at position 30 (attrval30met)), the age of onset ranges from the late 20s to the early 60s. |
2008-02-19 |
2023-08-12 |
Not clear |
| Bárbara Macedo, Ana Rita Batista, José Barbas do Amaral, Maria João Saraiv. Biomarkers in the assessment of therapies for familial amyloidotic polyneuropathy. Molecular medicine (Cambridge, Mass.). vol 13. issue 11-12. 2008-02-01. PMID:17932549. |
we previously demonstrated that in familial amyloidotic polyneuropathy (fap) related to the abnormal extracellular tissue deposition of mutant transthyretin (ttr), inflammatory and apoptotic pathways are triggered in the presymptomatic stages of the disease, when nonfibrillar ttr deposits are present. |
2008-02-01 |
2023-08-12 |
mouse |
| S D Santos, I Cardoso, J Magalhães, M J Saraiv. Impairment of the ubiquitin-proteasome system associated with extracellular transthyretin aggregates in familial amyloidotic polyneuropathy. The Journal of pathology. vol 213. issue 2. 2007-12-07. PMID:17724793. |
we have studied the ups in familial amyloidotic polyneuropathy (fap), a neurodegenerative disorder caused by extracellular deposition of mutant transthyretin (ttr). |
2007-12-07 |
2023-08-12 |
mouse |
| Yuko Motozaki, Yu Sugiyama, Chiho Ishida, Kiyonobu Komai, Shiro Matsubara, Masahito Yamad. Phenotypic heterogeneity in a family with FAP due to a TTR Leu58Arg mutation: a clinicopathologic study. Journal of the neurological sciences. vol 260. issue 1-2. 2007-12-06. PMID:17466336. |
a family with familial amyloid polyneuropathy (fap) due to a transthyretin (ttr) leu58arg mutation was investigated clinicopathologically. |
2007-12-06 |
2023-08-12 |
Not clear |
| Carolina E Fleming, Maria J Saraiva, Mónica M Sous. Transthyretin enhances nerve regeneration. Journal of neurochemistry. vol 103. issue 2. 2007-11-20. PMID:17897357. |
mutations in transthyretin (ttr) are associated with familial amyloid polyneuropathy, a neurodegenerative disorder characterized by ttr deposition in the pns. |
2007-11-20 |
2023-08-12 |
mouse |
| Carolina E Fleming, Maria J Saraiva, Mónica M Sous. Transthyretin enhances nerve regeneration. Journal of neurochemistry. vol 103. issue 2. 2007-11-20. PMID:17897357. |
moreover, the assignment of a ttr function in nerve biology and repair, may explain its preferential deposition, when mutated, in the pns of familial amyloid polyneuropathy patients. |
2007-11-20 |
2023-08-12 |
mouse |
| b' S Augustin, D Llige, A Andreu, A Gonz\\xc3\\xa1lez, J Genesc\\xc3\\xa. Familial amyloidosis in a large Spanish kindred resulting from a D38V mutation in the transthyretin gene. European journal of clinical investigation. vol 37. issue 8. 2007-11-19. PMID:17635579.' |
transthyretin amyloidosis, also known as familial amyloidotic polyneuropathy, is an autosomal dominant disorder that results from a mutation in the gene encoding plasma transthyretin (ttr). |
2007-11-19 |
2023-08-12 |
Not clear |
| Amir Said Alizadeh Naderi, Farnas Nematollah Farsian, Peter Igarash. Gastrointestinal amyloidosis associated with transthyretin Phe64Ser mutation. The American journal of the medical sciences. vol 334. issue 3. 2007-11-13. PMID:17873539. |
familial amyloidotic polyneuropathy (fap) is a hereditary generalized amyloidosis that results from mutations in the transthyretin (ttr) gene. |
2007-11-13 |
2023-08-12 |
Not clear |
| Malgorzata Pokrzywa, Ingrid Dacklin, Dan Hultmark, Erik Lundgre. Misfolded transthyretin causes behavioral changes in a Drosophila model for transthyretin-associated amyloidosis. The European journal of neuroscience. vol 26. issue 4. 2007-10-25. PMID:17714186. |
familial amyloidotic polyneuropathy is an autosomal dominant neurodegenerative disorder caused by accumulation of mutated transthyretin (ttr) amyloid fibrils in different organs and prevalently around peripheral nerves. |
2007-10-25 |
2023-08-12 |
drosophila_melanogaster |
| Idalina Beirão, Luísa Lobato, Paulo M P Costa, Isabel Fonseca, Manuela Silva, Fernanda Bravo, António Cabrita, Graça Port. Liver transplantation and anemia in familial amyloidosis ATTR V30M. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 14. issue 1. 2007-10-04. PMID:17453623. |
familial amyloid polyneuropathy type i (fap-i) is caused by a mutant transthyretin (ttr v30m) produced by liver, and orthotopic liver transplantation (olt) is a widely accepted treatment for stopping the major production of ttr v30m. |
2007-10-04 |
2023-08-12 |
Not clear |