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Porto, Portugal

The Abel Salazar Biomedical science Institute is a graduate medical and life science school of the University of Porto. The Institute is especially geared to scientific research and investigation.Along with traditional medicine, including specialities such as oncology, public health and mental health, it also teaches acupuncture, marine biology, veterinary medicine, biochemistry and bioengineering. It is named after Abel Salazar , a Portuguese physician, lecturer, researcher and painter who worked and lived in Porto.On the main hall of the Institute, the famous maxim of Abel Salazar can be read:"The one who only knows Medicine, not even Medicine does he know." Wikipedia.

Barreira Da Silva R.,University of Zurich | Barreira Da Silva R.,Abel Salazar Biomedical Sciences Institute | Munz C.,University of Zurich
Cellular and Molecular Life Sciences | Year: 2011

Natural killer (NK) cells have originally been identified by their spontaneous cytolytic potential against tumor cells, which, however, might result from pre-activation due to prior pathogen exposure. Resting NK cells, on the contrary, require activation by bystander antigen-presenting cells to reach their full functional competence. In this review, we will summarize studies on how dendritic cells (DCs), the most potent type of antigen-presenting cell, communicate with human NK cells to activate them in secondary lymphoid organs and to integrate signals from activated NK cells at sites of inflammation for their own maturation. Furthermore, we will review aspects of the immunological synapse, which mediates this cross-talk. These studies provide the mechanistic understanding of how mature DCs can activate NK cells and survive to go on for the activation of adaptive immunity. This feature of DCs, to activate different waves of immune responses, could be harnessed for immunotherapies, including vaccinations. © 2011 Springer Basel AG. Source

Miura S.K.,University of California at Los Angeles | Martins A.,University of California at Los Angeles | Martins A.,Abel Salazar Biomedical Sciences Institute | Zhang K.X.,University of California at Los Angeles | And 2 more authors.
Cell | Year: 2013

The Drosophila Dscam1 gene encodes a vast number of cell recognition molecules through alternative splicing. These exhibit isoform-specific homophilic binding and regulate self-avoidance, the tendency of neurites from the same cell to repel one another. Genetic experiments indicate that different cells must express different isoforms. How this is achieved is unknown, as expression of alternative exons in vivo has not been shown. Here, we modified the endogenous Dscam1 locus to generate splicing reporters for all variants of exon 4. We demonstrate that splicing does not occur in a cell-type-specific fashion, that cells sharing the same anatomical location in different individuals express different exon 4 variants, and that the splicing pattern in a given neuron can change over time. We conclude that splicing is probabilistic. This is compatible with a widespread role in neural circuit assembly through self-avoidance and is incompatible with models in which specific isoforms of Dscam1 mediate homophilic recognition between processes of different cells. © 2013 Elsevier Inc. Source

Goncalves A.P.,Abel Salazar Biomedical Sciences Institute
G3 (Bethesda, Md.) | Year: 2014

We pinpoint CZT-1 (cell death-activated zinc cluster transcription factor) as a novel transcription factor involved in tolerance to cell death induced by the protein kinase inhibitor staurosporine in Neurospora crassa. Transcriptional profiling of staurosporine-treated wild-type cells by RNA-sequencing showed that genes encoding the machinery for protein synthesis are enriched among the genes repressed by the drug. Functional category enrichment analyses also show that genes encoding components of the mitochondrial respiratory chain are downregulated by staurosporine, whereas genes involved in endoplasmic reticulum activities are upregulated. In contrast, a staurosporine-treated Δczt-1 deletion strain is unable to repress the genes for the respiratory chain and to induce the genes related to the endoplasmic reticulum, indicating a role for CZT-1 in the regulation of activity of these organelles. The Δczt-1 mutant strain displays increased reactive oxygen species accumulation on insult with staurosporine. A genome-wide association study of a wild population of N. crassa isolates pointed out genes associated with a cell death role of CZT-1, including catalase-1 (cat-1) and apoptosis-inducing factor-homologous mitochondrion-associated inducer of death 2 (amid-2). Importantly, differences in the expression of czt-1 correlates with resistance to staurosporine among wild isolate strains. Our results reveal a novel transcription factor that regulates drug resistance and cell death in response to staurosporine in laboratory strains as well as in wild isolates of N. crassa. Copyright © 2014 Gonçalves et al. Source

Tomas A.M.,University of Porto | Tomas A.M.,Abel Salazar Biomedical Sciences Institute | Castro H.,University of Porto
Antioxidants and Redox Signaling | Year: 2013

Significance: In the single mitochondrion of protozoan trypanosomatid parasites there are several sites for the generation and elimination of reactive oxygen species (ROS), a class of molecules that exhibit a dual role in cells, either as regulatory mediators or as cytotoxic effectors. Recent Advances: Formation of ROS in trypanosomatid mitochondria can be induced by various drug compounds. Importantly, it can also be triggered by specific physiologic stimuli, indicating that this phenomenon may occur in living parasites as well. Elimination of ROS in these organelles is attributed to the activity of two iron-dependent superoxide dismutases (FeSODs) and up to three different peroxidases (a cytochrome c peroxidase and two thiol peroxidases). Critical Issues: Data regarding the formation of ROS in trypanosomatid mitochondria are limited and nonsystematic. Another critical issue refers to the exact contribution of mitochondrial FeSODs and peroxidases for ROS removal, given that their antioxidant activity is not essential when abrogated individually. This suggests some level of functional overlapping or that ROS produced in mitochondria under normal conditions can be removed noncatalytically. Also still unsolved is the mechanism by which mitochondrial thiol peroxidases are regenerated to their reduced (active) form. Future Directions: The production of intramitochondrial ROS under physiologic conditions and their implication in parasite biology should be further clarified. The relative importance of enzymatic versus nonenzymatic mechanisms for ROS elimination in trypanosomatid mitochondria also requires investigation. Simultaneous depletion of several redundant antioxidant enzymes and determination of noncatalytic antioxidants are possible ways to achieve this. Antioxid. Redox Signal. 19, 696-707. © Copyright 2013, Mary Ann Liebert, Inc. 2013. Source

Vieira M.,Abel Salazar Biomedical Sciences Institute | Saraiva M.J.,IBMC Institute Biologia Molecular e Celular
FEBS Letters | Year: 2013

Transthyretin is the carrier protein of thyroxine and retinol in plasma and cerebrospinal fluid and has been described also as a neuroprotective molecule. 14-3-3 Proteins are very important in many cellular processes, being their absence related with deficits in memory and learning. The analysis of the relationship between these two proteins is the main objective of this work. We found that hippocampi of young TTR null mice presented lower levels of 14-3-3ζ protein, but no changes in gene expression when compared to TTR wild type littermates were noted. Cellular studies ascribed this finding to increased degradation of 14-3-3ζ in lysosomes in the absence of TTR, increasing autophagy. © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. Source

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