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A
Se, H. C., Leight, S. N., Lee, V. M. - Y., Li, T., et al. (2007). Accelerated Aβ deposition in APPswe/PS1ΔE9 mice with hemizygous deletions of TTR (transthyretin). Journal of Neuroscience, 27(26), 7006 - 7010.
Monteiro, F. A., Sousa, M. M., Cardoso, I., Do Amaral, J. B., et al. (2006). Activation of ERK1/2 MAP kinases in familial amyloidotic polyneuropathy. Journal of Neurochemistry, 97(1), 151 - 161.
Santos, S. D., Magalhães, J., & Saraiva, M. J. (2008). Activation of the heat shock response in familial amyloidotic polyneuropathy. Journal of Neuropathology and Experimental Neurology, 67(5), 449 - 455.
Westermark, P., Benson, M. D., Buxbaum, J. N., Cohen, A. S., et al. (2005). Amyloid: Toward terminology clarification: Report from the Nomenclature Committee of the International Society Of Amyloidosis. Amyloid, 12(1), 1 - 4.
Santos, S. D., Costa, R., Teixeira, P. F., Gottesman, M., et al. (2008). Amyloidogenic properties of transthyretin-like protein (TLP) from Escherichia coli. FEBS Letters, 582(19), 2893 - 2898.
Macedo, B., Batista, A. R., Ferreira, N., Almeida, M. R., & Saraiva, M. J. (2008). Anti-apoptotic treatment reduces transthyretin deposition in a transgenic mouse model of Familial Amyloidotic Polyneuropathy. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1782(9), 517 - 522.
Liz, M. A., Gomes, C. M., Saraiva, M. J., & Sousa, M. M. (2007). ApoA-I cleaved by transthyretin has reduced ability to promote cholesterol efflux and increased amyloidogenicity. Journal of Lipid Research, 48(11), 2385 - 2395.
C
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).
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.
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.
Almeida, M. R., & Saraiva, M. J. (2012). Clearance of extracellular misfolded proteins in systemic amyloidosis: Experience with transthyretin. FEBS Letters, 586(18), 2891 - 2896.
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.
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).
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.
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.
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.
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.
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.

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