Dr Theo Kantidakis completed his undergraduate studies at the Biology department of Aristotle University of Thessaloniki, Greece, in 2002. He continued his education in the UK, by attending the MSc in Molecular Genetics at the University of Leicester, from which he graduated with distinction in 2003. Subsequently, he secured a prestigious 4-year PhD prize scholarship from the Wellcome Trust at the University of Glasgow (2003-2007), which fully funded his MRes and PhD research.
During his PhD, Dr Kantidakis worked on multiple aspects of the regulation of RNA polymerase III transcription in the lab of Professor Bob White. He started his postdoctoral training at the Beatson Institute for Cancer Research (2008-2010) and showed how mTOR can affect tRNA transcription by phosphorylation of transcriptional repressor MAF1.
Next, Dr Kantidakis moved to Cancer Research UK’s London Research Institute (now Francis Crick Institute) to continue his postdoctoral studies (2010-2016) with Dr Jesper Svejstrup, working on the interface of RNA polymerase II transcription, chromatin epigenetics and the maintenance of genomic stability. By employing several of the latest genome-wide techniques, he discovered, among others, that inactivation of MLL2 (KMT2D), a histone methyltransferase that is often mutated in many cancers, results in transcription stress, DNA damage and genomic instability, providing a mechanism to explain its widespread role as a cancer driver.
In 2016, Dr Kantidakis moved to Xi’an Jiaotong-Liverpool University (XJTLU) in China, where he taught at the department of Biological Sciences. In 2018, He moved back to UK and joined the newly established Aston Medical School (AMS).
Dr Kantidakis research has been published in many prestigious journals, including Cell, Genes & Development, PNAS, Nucleic Acids Research. He is currently establishing his lab at AMS to pursue his research interests in chromatin and transcription regulation, investigating their role in DNA damage and genomic stability.
Williamson L, Saponaro M, Boeing S, East P, Mitter R, Kantidakis T, Kelly GP, Lobley A, Walker J, Spencer-Dene B, Howell M, Stewart A, Svejstrup JQ. UV Irradiation Induces a Non-coding RNA that Functionally Opposes the Protein Encoded by the Same Gene. Cell. 2017 Feb 23;168(5):843-855.e13. doi: 10.1016/j.cell.2017.01.019.
Kantidakis T, Saponaro M, Mitter R, Horswell S, Kranz A, Boeing S, Aygün O, Kelly GP, Matthews N, Stewart A, Stewart AF, Svejstrup JQ. Mutation of cancer driver MLL2 results in transcription stress and genome instability. Genes Dev. 2016 Feb 15;30(4):408-20. doi: 10.1101/gad.275453.115.
Saponaro M, Kantidakis T, Mitter R, Kelly GP, Heron M, Williams H, Söding J, Stewart A, Svejstrup JQ. RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress. Cell. 2014 May 22;157(5):1037-49. doi: 10.1016/j.cell.2014.03.048.
Kantidakis T, White RJ. A feedback loop between mTOR and tRNA expression? Cell Cycle. 2010 Aug 1;9(15):2934-5. doi: 10.4161/cc.9.15.12737.
Kantidakis T, Ramsbottom BA, Birch JL, Dowding SN, White RJ. mTOR associates with TFIIIC, is found at tRNA and 5S rRNA genes, and targets their repressor Maf1. Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):11823-8. doi: 10.1073/pnas.1005188107.
Kantidakis T, White RJ. Dr1 (NC2) is present at tRNA genes and represses their transcription in human cells. Nucleic Acids Res. 2010 Mar;38(4):1228-39. doi: 10.1093/nar/gkp1102.
Aran V, Brandie FM, Boyd AR, Kantidakis T, Rideout EJ, Kelly SM, Gould GW, Bryant NJ. Characterization of two distinct binding modes between syntaxin 4 and Munc18c. Biochem J. 2009 May 1;419(3):655-60. doi: 10.1042/BJ20082293.
Noubade R, Saligrama N, Spach K, Del Rio R, Blankenhorn EP, Kantidakis T, Milligan G, Rincon M, Teuscher C. Autoimmune disease-associated histamine receptor H1 alleles exhibit differential protein trafficking and cell surface expression. J Immunol. 2008 Jun 1;180(11):7471-9.
Goodfellow SJ, Graham EL, Kantidakis T, Marshall L, Coppins BA, Oficjalska-Pham D, Gérard M, Lefebvre O, White RJ. Regulation of RNA polymerase III transcription by Maf1 in mammalian cells. J Mol Biol. 2008 May 2;378(3):481-91. doi: 10.1016/j.jmb.2008.02.060.
Morton JP, Kantidakis T, White RJ. RNA polymerase III transcription is repressed in response to the tumour suppressor ARF. Nucleic Acids Res. 2007;35(9):3046-52.
Gomez-Roman N, Felton-Edkins ZA, Kenneth NS, Goodfellow SJ, Athineos D, Zhang J, Ramsbottom BA, Innes F, Kantidakis T, Kerr ER, Brodie J, Grandori C, White RJ. Activation by c-Myc of transcription by RNA polymerases I, II and III. Biochem Soc Symp. 2006;(73):141-54.
Fairley JA, Kantidakis T, Kenneth NS, Intine RV, Maraia RJ, White RJ. Human La is found at RNA polymerase III-transcribed genes in vivo. Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18350-5.
Woods AJ, Kantidakis T, Sabe H, Critchley DR, Norman JC. Interaction of paxillin with poly(A)-binding protein 1 and its role in focal adhesion turnover and cell migration. Mol Cell Biol. 2005 May;25(9):3763-73.
Google Scholar: https://scholar.google.co.uk/citations?user=GmI842QAAAAJ&hl=en
Browser does not support script.