OFFER DEADLINE01/07/2020 09:00 - Europe/Brussels
EU RESEARCH FRAMEWORK PROGRAMMEH2020 / Marie Skłodowska-Curie Actions
ORGANISATION/COMPANYInternational Research Projects Office
DEPARTMENTPromotion and Advisory Unit
Professor Pedro P. Medina Vico, from the Department of Biochemistry and Molecular Biology I at the University of Granada, welcomes postdoctoral candidates interested in applying for a Marie Skłodowska-Curie Individual Fellowships (MSCA-IF) in 2020 at this University. Please note that applicants must comply with the Mobility Rule (more information: http://sl.ugr.es/0aNV).
Brief description of the institution:
The University of Granada (UGR), founded in 1531, is one of the largest and most important universities in Spain. The UGR has been awarded with the "Human Resources Excellence in Research (HRS4R)", which reflects the UGR’s commitment to continuously improve its human resource policies in line with the European Charter for Researchers and the Code of Conduct for the Recruitment of Researchers. The UGR is also a leading institution in research, located in the top 5/10 of Spanish universities by a variety of ranking criteria, such as national R&D projects, fellowships awarded, publications, or international funding.
UGR is one of the few Spanish Universities listed in the Shanghai Top 500 ranking (http://sl.ugr.es/0aw0). The Academic Ranking of World Universities (ARWU) places the UGR in 268th position in the world and as the 4th highest ranked University in Spain, reaffirming its position as an institution at the forefront of national and international research. From the perspective of specialist areas in the ARWU rankings, the UGR is outstanding in Documentation (ranked in the 36th in the world) or Food science technology (ranked 37th in the world), Mathematics and Computer Science (ranked among the top 76-100 in the world).
The UGR has 4 researchers at the top of the Highly Cited Researchers (HCR) list in the Computer Science area. With regard to broader subject fields, the UGR is ranked in 45th position in the universities worldwide in the discipline of Engineering. It is also well recognized for its web presence (http://sl.ugr.es/0a6i) taking 36th place in the top 200 Universities in Europe. Internationally, we bet decidedly by our participation in the calls of the Framework Programme of the European Union. For the duration of the last two Framework Programmes, the UGR has obtained a total of 66 projects, with total funding of 18.02 million euros, and for H2020, 80 projects with total funding around 20.6 million euros.
Brief description of the Centre/Research Group
Group CTS-993. GENE EXPRESSION REGULATION increases the functional versatility and adaptability of the cell by allowing it to express certain proteins when needed. It is, therefore, one of the most important and complex processes of biology. Changes in the gene expression patterns are key in cancer cell transformation, through an increase in expression of genes that promote carcinogenesis (oncogenes) and/or a decrease in expression of genes that prevent it (tumour suppressor genes). Non-coding RNAs and chromatin-structure both play important roles in this process and have been found to be critical in the development of human pathologies. Both of these regulatory elements, especially in the context of CANCER, have been the focus of my interest during my career.
The SWI/SNF complex is an ATP-dependent chromatin-remodelling complex that is known to regulate EPIGENETICALLY the gene expression (Kwon, Imbalzano et al. 1994). Increasing evidence demonstrates that some components of the SWI/SNF complex are tumour suppressors and are involved in human cancer development. One subunit of this complex, SNF5, is inactivated in malignant rhabdoid tumours (MRTs) and heterozygous Snf5 knockout mice develop tumours that are histologically similar to human MRTs (Roberts, Galusha et al. 2000; Roberts, Leroux et al. 2002). BRG1 (Medina and Sanchez-Cespedes 2008), the helicase/ATPase catalytic subunits of the SWI/SNF complex, is mutated in many different cancer cell lines (Wong, Shanahan et al. 2000; Medina, Romero et al. 2008). Additionally, germline BRG1 mutations linked to a Rhabdoid Tumour Predisposition Syndrome was reported in a family, strongly suggesting that is a bona fide tumour suppressor gene (Schneppenheim, Fruhwald et al.). Recently, it has been discovered that two other subunits of the chromatin-remodelling complex, BAF250 (ARID1A) and BAF180 (PBRM1) (Jones, Wang et al. ; Wiegand, Shah et al. ; Varela, Tarpey et al. 2011; Wilson and Roberts 2011), are frequently mutated in ovarian clear cell carcinoma and renal carcinoma, respectively. All these observations support an important role of the SWI/SNF complex in cancer, however its specific function is still unclear.
MiRNAs are a recently discovered class of small RNA molecules that regulate gene expression at the post-transcriptional level. Due to their small size and unusual nature, miRNAs were not discovered in humans until 2000. Today, over one thousand miRNAs have been identified in the human genome. Aberrant biogenesis and/or expression of miRNAs have been linked to human diseases including cancer (Medina and Slack 2008). During my training as a postdoc in this field I have helped to reveal the critical role played by specific miRNAs in cancer. While most previous studies in the field used cell lines or in vitro systems, we pioneered the functional study of the role of miRNAs using in vivo transgenic mouse models. We demonstrated the therapeutic utility of let-7 microARN ectopic expression in vivo (Medina, Trang et al. 2010), and the important of a single microARNs (miR-21) to the drive of tumor development (Medina, Nolde et al. 2010). In my recently created group at the GenyO Center we will continue unveiling the role of the microRNAs and other non-coding RNA species in cancer with the hope to find novel and useful cancer therapies.
Life Sciences (LIFE)
For a correct evaluation of your candidature, please send the documents below to Professor Pedro P. Medina Vico (email@example.com):
- Letter of recommendation (optional)
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