Search

Your search keyword '"Prado, Marco Antônio M."' showing total 15 results
Start Over Author "Prado, Marco Antônio M."
15 results on '"Prado, Marco Antônio M."'

1. Alpha-7 Nicotinic Receptor Agonist Protects Mice Against Pulmonary Emphysema Induced by Elastase

Author

Banzato, Rosana, Pinheiro-Menegasso, Nathalia M., Novelli, Fernanda Paula Roncon Santana, Olivo, Clarice R., Taguchi, Laura, de Oliveira Santos, Stheffany, Fukuzaki, Silvia, Teodoro, Walcy Paganelli Rosolia, Lopes, Fernanda D. T. Q. S., Tibério, Iolanda F. L. C., de Toledo-Arruda, Alessandra Choqueta, Prado, Marco Antônio M., Prado, Vânia F., and Prado, Carla M.

Published
2024
Full Text
View/download PDF

4. Effects of VAChT reduction and α7nAChR stimulation by PNU-282987 in lung inflammation in a model of chronic allergic airway inflammation

Author

Pinheiro, Nathalia M., primary, Miranda, Claudia J.C.P., additional, Santana, Fernanda R., additional, Bittencourt-Mernak, Marcia, additional, Arantes-Costa, Fernanda M., additional, Olivo, Clarice, additional, Perini, Adenir, additional, Festa, Sérgio, additional, Caperuto, Luciana C., additional, Tibério, Iolanda F.L.C., additional, Prado, Marco Antônio M., additional, Martins, Mílton A., additional, Prado, Vânia F., additional, and Prado, Carla M., additional

Published
2020
Full Text
View/download PDF

7. Vesicular acetylcholine transport deficiency potentiates some inflammatory responses induced by diesel exhaust particles

Author

Santana, Fernanda P.R., primary, Pinheiro, Nathalia M., additional, Bittencourt-Mernak, Márcia I., additional, Perini, Adenir, additional, Yoshizaki, Kelly, additional, Macchione, Mariângela, additional, Saldiva, Paulo H.N., additional, Martins, Milton A., additional, Tibério, Iolanda F.L.C., additional, Prado, Marco Antônio M., additional, Prado, Vânia F., additional, and Prado, Carla M., additional

Published
2019
Full Text
View/download PDF

9. Pulmonary Inflammation Is Regulated by the Levels of the Vesicular Acetylcholine Transporter

Author

Pinheiro, Nathalia M., primary, Miranda, Claudia J. C. P., additional, Perini, Adenir, additional, Câmara, Niels O. S., additional, Costa, Soraia K. P., additional, Alonso-Vale, Maria Isabel C., additional, Caperuto, Luciana C., additional, Tibério, Iolanda F. L. C., additional, Prado, Marco Antônio M., additional, Martins, Mílton A., additional, Prado, Vânia F., additional, and Prado, Carla M., additional

Published
2015
Full Text
View/download PDF

15. Towards cellular receptors for prions.

Author

Lee KS, Linden R, Prado MA, Brentani RR, and Martins VR

Subjects
Humans, PrPSc Proteins metabolism, Prion Diseases pathology, Protein Isoforms, Signal Transduction immunology, PrPC Proteins metabolism, PrPSc Proteins pathogenicity, Prion Diseases metabolism, Receptors, Cell Surface metabolism
Abstract

Transmissible spongiform encephalopathies (TSE) are attributed to the conversion of the cellular prion protein (PrP(c)) into an abnormal isoform (PrP(sc)). This can be caused by the invasion of living organisms by infectious particles, or be inherited due to mutations on the PrP(c) gene. One of the most intriguing problems of prion biology is the inability to generate the infectious agent in vitro. This argues strongly that other cellular proteins besides those added in test tubes or found in cellular preparations are necessary for infection. Despite recent progress in the understanding of prion pathology, the subcellular compartments in which the interaction and conversion of PrP(c) into PrP(sc) take place are still controversial. PrP(c) interacts with various macromolecules at the cell membrane, in endocytic compartments and in the secretory pathway, all of which may play specific roles in the internalisation of PrP(sc) and conversion of PrP(c). A specific interacting protein required for the propagation of prions was originally proposed as a prion receptor, and later referred to as a ligand, a cofactor, protein X, or a partner. However, current studies indicate that PrP(c) associates with multi-molecular complexes, which mediate a variety of functions in distinct cellular compartments. It is proposed that a deeper understanding of the mechanics of such interactions, coupled to a better knowledge of the corresponding signalling pathways and ensuing cellular responses, will have a major impact on the prevention and treatment of TSE., (Copyright 2003 John Wiley & Sons, Ltd.)

Published
2003
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results