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Investigation
Bacterial Genetics
Research projects
Content with Investigacion .
- Título: Desvelando la genómica de las bacterias anaerobias procedentes de bacteriemias
Referencia Proyecto: PID202-1127477OB-I00-MPY 302/22.
Entidad financiador: Agencia Estatal de Investigación.
Fechas de ejecución: 2023-2026
Financiación 108.900 €.
Investigadora principal: Sylvia Valdezate
- Título: Plataformas MALDI-TOF/CMI SENSITITRETM Personal Técnico Apoyo
Referencia: PTA2019-016623-I.
Entidad Financiadora: Agencia Estatal de Investigación.
Fechas ejecución 12/2020-11/2023
Investigadora principal: Sylvia Valdezate
- Título: Elementos genéticos móviles protagonistas en la evolución de los serotipos pandémicos M1 y M89 de Streptococcus pyogenes en el síndrome del shock tóxico y otras infecciones invasivas
Referencia: (MPY 377/18).
Entidad financiadora: Instituto de Salud Carlos III. Agencia Estatal de Investigación en Salud Intramural (AESI).
Fechas de ejecución: 11/2018-12/2022.
Financiación: 40.000 €.
Investigadoras principales: Pilar Villalón. Co-IP Sylvia Valdezate.
- Título: Plataformas genéticas y su influencia en la resistencia a co-trimoxazol, macrólidos y tetraciclina en Nocardia spp.
Referencia: MPY 1278/15
Entidad financiadora: Instituto de Salud Carlos III. Agencia Estatal de Investigación en Salud Intramural (AESI).
Fechas de ejecución: 2015-2017.
Financiación: 88.141,8 €.
Investigadora principal: Sylvia Valdezate
- Título: Filogenia y caracterización de mecanismos moleculares de resistencia en Nocardia spp.
Referencia: MPY 1446/11
Entidad financiadora: Instituto de Salud Carlos III. Fondo de Investigación Sanitaria (AES). ()
Fechas de ejecución: 04/2012-10/2015
Financiación: 115.457 €.
Investigadora principal: Sylvia Valdezate.
- Título: Iberian network of laboratories of biological alert. Accreditation of methods for detection highly pathogenic agents (IB-BIOALERTNET).
Entidad financiadora: COMISIÓN EUROPEA HOME/2012/ISEC/AG/CBRN/4000003810. (Instituto de Salud Carlos III (VISAVET, IVIA, INSA, INIAV))
Referencia: SAFI 1132/13-7.
Fecha de ejecución: 2013-2015.
Financiación: 699.175 €.
Tipo de participación: Miembro del equipo investigador.
- Título: EQUATOX Project Establishment of Quality Assurances for theDetection of Biological Toxins of potential Bioterrorism risk.
Entidad financiadora y convocatoria: Seven Framework Programme for Research FP7-SECURITY. (Robert Koch-Institut Berlin Alemania).
Referencia: SEC-2011.5.4-1.
Fechas de ejecución: 2012-2014.
Publications
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 DOIContent with Investigacion .
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Mónica Valiente Novillo
Técnico de laboratorio. Convocatoria empleo juvenial (PEJ-2021-TL_BMD-21100)
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Noelia Castrillo Garrido
Técnico de Laboratorio. Contratada de Proyecto PID2021-127477OB-I00 (AEI)
ORCID code: 0000-0003-1676-9693
List of staff
Additional 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.