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Journal Article
Andrade, E. B., Alves, J., Madureira, P., Oliveira, L., et al. (2013). TLR2-induced IL-10 production impairs neutrophil recruitment to infected tissues during neonatal bacterial sepsis. Journal of Immunology, 191(9), 4759 - 4768.
Dinis, M., Tavares, D., Fonseca, A. J. M. M., Faria, R., et al. (2004). Therapeutic vaccine against Streptococcus sobrinus-induced caries. Journal of Dental Research, 83(4), 354 - 358.
Madureira, P., Baptista, M., Vieira, M., Magalhães, V., et al. (2007). Streptococcus agalactiae GAPDH is a virulence-associated immunomodulatory protein. Journal of Immunology, 178(3), 1379 - 1387.
Barradas, P. F., Vilhena, H., Oliveira, A. C., Granada, S., et al. (2017). Serological and molecular detection of spotted fever group Rickettsia in a group of pet dogs from Luanda, Angola. Parasites and Vectors, 10(1).
Vilanova, M., Teixeira, L., Caramalho, Í., Torrado, E., et al. (2004). Protection against systemic candidiasis in mice immunized with secreted aspartic proteinase 2. Immunology, 111(3), 334 - 342.
Dinis, M., Tavares, D., Veiga-Malta, I., Fonseca, A. J. M. M., et al. (2009). Oral therapeutic vaccination with Streptococcus sobrinus recombinant enolase confers protection against dental caries in rats. Journal of Infectious Diseases, 199(1), 116 - 123.
Trigo, G., Dinis, M., França, Â., Andrade, E. B., et al. (2009). Leukocyte populations and cytokine expression in the mammary gland in a mouse model of Streptococcus agalactiae mastitis. Journal of Medical Microbiology, 58(7), 951 - 958.
Magalhães, V., Veiga-Malta, I., Almeida, M. R., Baptista, M., et al. (2007). Interaction with human plasminogen system turns on proteolytic activity in Streptococcus agalactiae and enhances its virulence in a mouse model. Microbes and Infection, 9(11), 1276 - 1284.
Madureira, P., Andrade, E. B., Gama, B., Oliveira, L., et al. (2011). Inhibition of IL-10 production by maternal antibodies against group b streptococcus GAPDH confers immunity to offspring by favoring neutrophil recruitment. PLoS Pathogens, 7(11).
Camejo, A., Buchrieser, C., Couvé, E., Carvalho, F., et al. (2009). In vivo transcriptional profiling of Listeria monocytogenes and mutagenesis identify new virulence factors involved in infection. PLoS Pathogens, 5(5).
Veiga-Malta, I., Duarte, M., Dinis, M., Madureira, P., et al. (2004). Identification of NAD+ Synthetase from Streptococcus sobrinus as a B-Cell-Stimulatory Protein. Journal of Bacteriology, 186(2), 419 - 426.
Trigo, G., Ferreira, P., Ribeiro, N., Dinis, M., et al. (2008). Identification of immunoreactive extracellular proteins of Streptococcus agalactiae in bovine mastitis. Canadian Journal of Microbiology, 54(11), 899 - 905.
Magalhães, V., Andrade, E. B., Alves, J., Ribeiro, A., et al. (2013). Group B Streptococcus Hijacks the Host Plasminogen System to Promote Brain Endothelial Cell Invasion. PLoS ONE, 8(5).
Oliveira, L., Madureira, P., Andrade, E. B., Bouaboud, A., et al. (2012). Group B streptococcus GAPDH is released upon cell lysis, associates with bacterial surface, and induces apoptosis in murine macrophages. PLoS ONE, 7(1).
Veiga-Malta, I., Duarte, M., Dinis, M., Tavares, D., et al. (2004). Enolase from Streptococcus sobrinus is an immunosuppressive protein. Cellular Microbiology, 6(1), 79 - 88.
Dinis, M., Trigo, G., Chaves, N., Fonseca, A. J. M. M., et al. (2011). eEnolase maternal immunization confers caries protection on offspring. Journal of Dental Research, 90(3), 325 - 330.
Pereira, P. S., Teixeira, A., Pinho, S., Ferreira, P., et al. (2006). E-cadherin missense mutations, associated with hereditary diffuse gastric cancer (HDGC) syndrome, display distinct invasive behaviors and genetic interactions with the Wnt and Notch pathways in Drosophila epithelia. Human Molecular Genetics, 15(10), 1704 - 1712.
Teixeira, L., Marques, A., Meireles, C. S., Seabra, A. R., et al. (2005). Characterization of the B-cell immune response elicited in BALB/c mice challenged with Neospora caninum tachyzoites. Immunology, 116(1), 38 - 52.
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.

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