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Cytotoxic cell populations developed during treatment with tyrosine kinase inhibitors protect autologous CD4+ T cells from HIV-1 infection
Cytotoxic cell populations developed during treatment with tyrosine kinase inhibitors protect autologous CD4+ T cells from HIV-1 infection. Vigón L, Rodríguez-Mora S, Luna A, Sandonís V, Mateos E, Bautista G, Steegmann JL, Climent N, Plana M, Pérez-Romero P, de Ory F, Alcamí J, García-Gutierrez V, Planelles V, López-Huertas MR, Coiras M (AC). Biochem Pharmacol. 2020 Dec;182:114203. doi: 10.1016/j.bcp.2020.114203. PMID: 32828803.
PUBMED DOITyrosine Kinase Inhibition: a New Perspective in the Fight against HIV
Tyrosine Kinase Inhibition: a New Perspective in the Fight against HIV. Rodríguez-Mora S, Spivak AM, Szaniawski MA, López-Huertas MR, Alcamí J, Planelles V, Coiras M (AC). Curr HIV/AIDS Rep. 2019 Oct;16(5):414-422. doi: 10.1007/s11904-019-00462-5. PMID: 31506864. Review.
PUBMED DOIDasatinib protects humanized mice from acute HIV-1 infection
Dasatinib protects humanized mice from acute HIV-1 infection. Salgado M, Martinez-Picado J, Gálvez C, Rodríguez-Mora S, Rivaya B, Urrea V, Mateos E, Alcamí J, Coiras M (AC). Biochem Pharmacol. 2020 Apr;174:113625. doi: 10.1016/j.bcp.2019.113625. PMID: 31476293.
PUBMED DOIEvaluation of resistance to HIV-1 infection ex vivo of PBMCs isolated from patients with chronic myeloid leukemia treated with different tyrosine kinase inhibitors.
Evaluation of resistance to HIV-1 infection ex vivo of PBMCs isolated from patients with chronic myeloid leukemia treated with different tyrosine kinase inhibitors. Bermejo M, Ambrosioni J, Bautista G, Climent N, Mateos E, Rovira C, Rodríguez-Mora S, López-Huertas MR, García-Gutiérrez V, Steegmann JL, Duarte R, Cervantes F, Plana M, Miró JM, Alcamí J, Coiras M (AC). Biochem Pharmacol. 2018 Oct;156:248-264. doi: 10.1016/j.bcp.2018.08.031. PMID: 30142322.
PUBMED DOIAdditional Information
Streptococcus pneumoniae is a human pathogen that, despite the development of vaccines, continues to be an important cause of mortality and morbidity. We investigate the mechanisms of antibiotic resistance in this bacterium. On the one hand by identifying new therapeutic targets and on the other hand by investigating the molecular basis of the action of antibiotics already used in clinical practice (the fluoroquinolones levofloxacin and moxifloxacin) or not yet used (seconeolitsine). For this purpose, we used a multidisciplinary analysis involving genomics, transcriptomics and proteomics to understand the organization of the S. pneumoniae chromosome and the identification of the factors that stabilize this organization, including ncRNAs. Changes in the level of global supercoiling, either by inhibition of gyrase (decrease) or by inhibition of topoisomerase I (increase) alter the transcriptome. The modulated genes are located in domains, whose genes show specific functional characteristics. The aim is to identify new factors essential for S. pneumoniae physiology and to characterize transcriptional regulation in response to topological stress. In addition, RNA interference technology and CRISPR systems will be used as novel antibacterials. These studies will establish the bases for translational research aimed at the development of new therapeutic targets for the treatment of pneumococcal diseases.
Streptococcus pneumoniae is a human pathogen that, despite the development of vaccines, continues to be an important cause of mortality and morbidity. We investigate the mechanisms of antibiotic resistance in this bacterium. On the one hand by identifying new therapeutic targets and on the other hand by investigating the molecular basis of the action of antibiotics already used in clinical practice (the fluoroquinolones levofloxacin and moxifloxacin) or not yet used (seconeolitsine). For this purpose, we used a multidisciplinary analysis involving genomics, transcriptomics and proteomics to understand the organization of the S. pneumoniae chromosome and the identification of the factors that stabilize this organization, including ncRNAs. Changes in the level of global supercoiling, either by inhibition of gyrase (decrease) or by inhibition of topoisomerase I (increase) alter the transcriptome. The modulated genes are located in domains, whose genes show specific functional characteristics. The aim is to identify new factors essential for S. pneumoniae physiology and to characterize transcriptional regulation in response to topological stress. In addition, RNA interference technology and CRISPR systems will be used as novel antibacterials. These studies will establish the bases for translational research aimed at the development of new therapeutic targets for the treatment of pneumococcal diseases.