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Journal Article
Vieira, M., Leal, S. S., Gomes, C. M., & Saraiva, M. J. (2016). Evidence for synergistic action of transthyretin and IGF-I over the IGF-I receptor. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1862(4), 797 - 804.
Ferreira, N., Saraiva, M. J., & Almeida, M. R. (2012). Epigallocatechin-3-gallate as a potential therapeutic drug for TTR-related amyloidosis: "In vivo" evidence from FAP mice models. PLoS ONE, 7(1).
Santos, S. D., & Saraiva, M. J. (2004). Enlarged ventricles, astrogliosis and neurodegeneration in heat shock factor 1 null mouse brain. Neuroscience, 126(3), 657 - 663.
Teixeira, P. F., Cerca, F., Santos, S. D., & Saraiva, M. J. (2006). Endoplasmic reticulum stress associated with extracellular aggregates: Evidence from transthyretin deposition in familial amyloid polyneuropathy. Journal of Biological Chemistry, 281(31), 21998 - 22003.
Gonçalves, P., Martins, H., Costelha, S., & Saraiva, M. J. (2017). Efficiency of siRNA for removal of transthyretin V30M in a TTR leptomeningeal animal model. Amyloid, 24, 38 - 39.
Gonçalves, P., Martins, H., Costelha, S., Maia, L. F., & Saraiva, M. J. (2016). Efficiency of silencing RNA for removal of transthyretin V30M in a TTR leptomeningeal animal model. Amyloid, 23(4), 249 - 253.
Teixeira, C., Costelha, S., Martins, H. S., Teixeira, A., & Saraiva, M. J. (2017). Doxycycline-tauroursodeoxycholic acid treatment: effects in the heart of a transthyretin V30M transgenic mouse model. Amyloid, 24, 80.
Obici, L., Cortese, A., Lozza, A., Lucchetti, J., et al. (2012). Doxycycline plus tauroursodeoxycholic acid for transthyretin amyloidosis: A phase II study. Amyloid, 19(SUPPL. 1), 34 - 36.
Cardoso, I., & Saraiva, M. J. (2006). Doxycycline disrupts transthyretin amyloid: Evidence from studies in a FAP transgenic mice model. FASEB Journal, 20(2), 234 - 239.
Pires, R. H., Karsai, Á., Saraiva, M. J., Damas, A. M., & Kellermayer, M. S. Z. (2012). Distinct Annular Oligomers Captured along the Assembly and Disassembly Pathways of Transthyretin Amyloid Protofibrils. PLoS ONE, 7(9).
Gonçalves, N. P., Moreira, J., Martins, D., Vieira, P., et al. (2017). Differential expression of Cathepsin E in transthyretin amyloidosis: From neuropathology to the immune system. Journal of Neuroinflammation, 14(1).
Ferreira, N., Santos, S. A. O., Domingues, M. R. M., Saraiva, M. J., & Almeida, M. R. (2013). Dietary curcumin counteracts extracellular transthyretin deposition: Insights on the mechanism of amyloid inhibition. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1832(1), 39 - 45.
Rocha, S., Cardoso, I., Börner, H., Pereira, M. C., et al. (2009). Design and biological activity of β-sheet breaker peptide conjugates. Biochemical and Biophysical Research Communications, 380(2), 397 - 401.
Sousa, M. M., Ferraõ, J., Fernandes, R., Guimarães, A., et al. (2004). Deposition and passage of transthyretin through blood-nerve barrier in recipients of familial amyloid polyneuropathy livers. Laboratory Investigation, 84(7), 865 - 873.
Ferreira, N., Gonçalves, N. P., Saraiva, M. J., & Almeida, M. R. (2016). Curcumin: A multi-Target disease-modifying agent for late-stage transthyretin amyloidosis. Scientific Reports, 6.
Santos, S. D., Lambertsen, K. L., Clausen, B. H., Akinc, A., et al. (2010). CSF transthyretin neuroprotection in a mouse model of brain ischemia. Journal of Neurochemistry, 115(6), 1434 - 1444.
Morais-De-Sá, E., Pereira, P. J. B., Saraiva, M. J., & Damas, A. M. (2004). The crystal structure of transthyretin in complex with diethylstilbestrol: A promising template for the design of amyloid inhibitors. Journal of Biological Chemistry, 279(51), 53483 - 53490.
Saraiva, A. M., Cardoso, I., Pereira, M. C., Coelho, M. A. N., et al. (2010). Controlling amyloid-β peptide(1-42) oligomerization and toxicity by fluorinated nanoparticles. ChemBioChem, 11(13), 1905 - 1913.
Cardoso, I., Almeida, M. R., Ferreira, N., Arsequell, G., et al. (2007). Comparative in vitro and ex vivo activities of selected inhibitors of transthyretin aggregation: Relevance in drug design. Biochemical Journal, 408(1), 131 - 138.
Ohmori, H., Ando, Y., Makita, Y., Onouchi, Y., et al. (2004). Common origin of the Val30Met mutation responsible for the amyloidogenic transthyretin type of familial amyloidotic polyneuropathy. Journal of medical genetics, 41(4).
Magalhães, J., & Saraiva, M. J. (2011). Clusterin overexpression and its possible protective role in transthyretin deposition in familial amyloidotic polyneuropathy. Journal of Neuropathology and Experimental Neurology, 70(12), 1097 - 1106.
Almeida, M. R., & Saraiva, M. J. (2012). Clearance of extracellular misfolded proteins in systemic amyloidosis: Experience with transthyretin. FEBS Letters, 586(18), 2891 - 2896.
Sant'Anna, R., Almeida, M. R., Varejao, N., Gallego, P., et al. (2017). Cavity filling mutations at the thyroxine-binding site dramatically increase transthyretin stability and prevent its aggregation. Scientific Reports, 7.
Macedo, B., Magalhães, J., Batista, A. R., & Saraiva, M. J. (2010). Carvedilol treatment reduces transthyretin deposition in a familial amyloidotic polyneuropathy mouse model. Pharmacological Research, 62(6), 514 - 522.
Panayiotou, E., Fella, E., Papacharalambous, R., Malas, S., et al. (2017). C1q ablation exacerbates amyloid deposition: A study in a transgenic mouse model of ATTRV30M amyloid neuropathy. PLoS ONE, 12(4).


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