Jose Miguel Lizcano  de Vega
  • Biography
  • I received my PhD degree (Biochemistry) at the UAB. After completing my training at the of Prof. Keith F Tipton’s Laboratory (Trinity College Dublin, Ireland, 1995-96), I moved to the MRC Protein Phosphorylation Unit at the University of Dundee (UK), to work as a MRC Research Associate with Professors Sir Philip Cohen and Dario Alessi (1998-2004). I focussed my research on the study of cellular signalling pathways ruled by new protein kinases that play key roles in driving pathologies, such as diabetes and cancer. In 2004, I obtained a Ramón y Cajal Tenure Track Position at the UAB Institut de Neurociències, where I founded the Protein Kinases in Cancer Research Laboratory. From 2005, I am Associate Professor at the UAB Department of Biochemistry & Molecular Biology, where I acted as Deputy Director (2008-2014). From 2016 I am Coordinator of the Biochemistry Unit at the UAB School of Medicine.
    Research Interest:
    My Lab is interested in dissecting new cellular signaling pathways that control cancer cell proliferation and differentiation. We study the new protein kinases ERK5 (the newest MAP kinase), the tumor suppressor LKB1 and the Akt-mTORC1 pathway. We use two different perspectives to approach fundamental problems:
    1. Basic Research. Dissection of the mechanisms by which LKB1, Akt and ERK5 kinases exert control on proliferation and survival of tumor cells. We have contributed to propose new molecular mechanism for regulation of protein kinase Akt; discovered that tumor suppressor kinase LKB1 functions as a master kinase; or more recently, we have established a new mechanism for ERK5 nuclear translocation and regulation of tumor cell proliferation regardless of its enzymatic activity.
    2. Research directed to pharmacological intervention in cancer. We are involved in potentiating translational aspects of our resources. We established collaboration with Biotech Companies. Since 2011, we actively collaborate with Ability Pharmaceuticals SL in the preclinical/clinical development of the new antitumor drug ABTL0812, which successfully finished first-in-humans, Phase I/Ib Clinical Trial (NCT02201823) in patients with advanced solid tumors. We have discovered a new cellular signaling pathway by which ABTL0812 exerts its antitumor action: ABTL0812 activates PPAR-mediated transcription of TRIB3 pseudokinase, which in turn binds and inhibits Akt resulting in mTORC1 inhibition, growth arrest and autophagy-mediated cancer cell death. Finally, we actively collaborate with other academic laboratories characterizing new ERK5 inhibitors that show anti-tumor activity.
  • Research groups
  • Protein Kinases in Cancer Research
  • Publications
  • Muñoz-Guardiola et al. Autophagy 2020. doi: 10.1080/15548627.2020.1761651
    Ferguson et al. 2020. Nature Chemical Biology 16:635-643. doi: 10.1038/s41589-020-0506-0
    Hermanova et al. 2020. J Experimental Medicine. doi: 10.1084/jem.20191787.
    Erazo et al. 2020. J Inter Mol Sci. 21(6). pii: E2203. doi: 10.3390/ijms21062203.
    Erazo et al. 2016. Clin Cancer Research 22: 2508-16. doi: 10.1158/1078-0432.CCR-15-1808
    Gomez et al. 2016 Frontiers Cell Development Biology doi: 10.3389/fcell.2016.00105
    Erazo et al. 2013. Molecular & Cellular Biology 33:1671-86. doi: 10.1128/MCB.01246-12
    Lizcano et al.  2004. EMBO Journal 23: 833-43
    Biondi et al. 2004. EMBO Journal 21: 4219-28
  • More information
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    ORCID: 0000-0002-3154-5383




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