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- Relatório REVIVE 2011-2015 - Culicídeos e Ixodídeos: Rede de Vigilância de VetoresPublication . Centro de Estudos de Vetores e Doenças Infeciosas Doutor Francisco CambournacRelatório – Culicídeos e Ixodídeos, relativo ao ano de 2015 e a sua evolução nos últimos 5 anos (2011-2015), elaborado no âmbito das atividades desenvolvidas no 2.º protocolo REVIVE – Rede de Vigilância de Vetores (2011-2015). O programa REVIVE resulta da colaboração entre instituições do Ministério da Saúde (Direção-Geral da Saúde, Administrações Regionais de Saúde e Instituto Nacional de Saúde), devendo-se a sua criação, sobretudo, à necessidade de instalar capacidades para melhorar o conhecimento sobre as espécies de vetores presentes no país, a sua distribuição e abundância, esclarecer o seu papel como vetor de agentes de doença, assim como detetar atempadamente introduções de espécies invasoras com importância em saúde pública.
- New insights into host-parasite ubiquitin proteome dynamics in P. falciparum infected red blood cells using a TUBEs-MS approachPublication . Mata-Cantero, L.; Azkargorta, M.; Aillet, F.; Xolalpa, W.; LaFuente, M.J.; Elortza, F.; Carvalho, A.S.; Martin-Plaza, J.; Matthiesen, Rune; Rodriguez, M.S.Malaria, caused by Plasmodium falciparum (P. falciparum), ranks as one of the most baleful infectious diseases worldwide. New antimalarial treatments are needed to face existing or emerging drug resistant strains. Protein degradation appears to play a significant role during the asexual intraerythrocytic developmental cycle (IDC) of P. falciparum. Inhibition of the ubiquitin proteasome system (UPS), a major intracellular proteolytic pathway, effectively reduces infection and parasite replication. P. falciparum and erythrocyte UPS coexist during IDC but the nature of their relationship is largely unknown. We used an approach based on Tandem Ubiquitin-Binding Entities (TUBEs) and 1D gel electrophoresis followed by mass spectrometry to identify major components of the TUBEs-associated ubiquitin proteome of both host and parasite during ring, trophozoite and schizont stages. Ring-exported protein (REX1), a P. falciparum protein located in Maurer's clefts and important for parasite nutrient import, was found to reach a maximum level of ubiquitylation in trophozoites stage. The Homo sapiens (H. sapiens) TUBEs associated ubiquitin proteome decreased during the infection, whereas the equivalent P. falciparum TUBEs-associated ubiquitin proteome counterpart increased. Major cellular processes such as DNA repair, replication, stress response, vesicular transport and catabolic events appear to be regulated by ubiquitylation along the IDC P. falciparum infection.
- Expression of tumor-related Rac1b antagonizes B-Raf-induced senescence in colorectal cellsPublication . Henriques, Andreia; Barros, Patrícia; Matos, Paulo; Jordan, PeterMutations in the BRAF oncogene have been identified as a tumor-initiating genetic event in mainly melanoma, thyroid and colon cancer, resulting in an initial proliferative stimulus that is followed by a growth arrest period known as oncogene-induced senescence (OIS). It remains unknown what triggers subsequent escape from OIS to allow further tumor progression. A previous analysis revealed that overexpression of splice variant Rac1b occurs in around 80% of colorectal tumors carrying a mutation in BRAF. Using both BRaf-V600E-directed RNAi and overexpression we demonstrate that this mutation does not directly lead to Rac1b overexpression, indicating the latter as an independent event during tumor progression. Nonetheless, we observed that expression of oncogenic BRaf-V600E in non-transformed colonocytes (NCM460 cell line) increased both the transcript and protein levels of p14ARF, p15INK4b and p21CIP1 and led to increased expression of β-galactosidase, all indicators of OIS induction. Interestingly, whereas the protein levels of these markers were reduced upon Rac1b overexpression, the levels of their respective transcripts remained unchanged. Importantly, the co-expression of Rac1b with B-Raf-V600E reverted the OIS phenotype, reducing the expression levels of the cell-cycle inhibitors and β-galactosidase to those of control cells. These data identify increased Rac1b expression as one potential mechanism by which colorectal tumor cells can escape from B-Raf-induced OIS.