Tee, Andrew - Cardiff University

个人简介

Education and Qualifications: 1998 B.Sc. Hons Biochemistry (i) first class Dundee University (Dundee, United Kingdom) 2001 Ph.D. Biochemistry Dundee University (Dundee, United Kingdom) Career Overview: 2012 - present Senior Lecturer, Principle Investigator, Division of Cancer and Genetics, Cardiff University 2007 - 2012 Non-Clinical Research Lecturer, Principle Investigator, Institute of Medical Genetics, Cardiff University 2004 - 2007 Independent investigator, Laboratory of Prof. Grahame D. Hardie, University of Dundee, 2001 - 2004 Postdoctoral Fellow, Laboratory of Prof. John Blenis, Harvard Medical School, Boston, MA. 1998 - 2001 Ph.D. student, Laboratory of Prof. Christopher G. Proud, University of Dundee

研究领域

Tuberous Sclerosis Complex I became interested in TSC at Harvard, where I was involved in a number of key studies on the upstream control of mTOR by insulin/PI 3-kinase and protein kinase B (PKB/Akt), and by the small G-protein Rheb. I identified the TSC gene product, TSC2 as a direct substrate for PKB/Akt as well as a downstream target within the mitogen activated protein kinase (MAPK) pathway. I also discovered that the TSC1/2 heterodimer specifically inhibited signalling through mTOR, and that this was due to the increased GTPase activity towards novel small G-proteins called Rheb and RhebL1. I am considered a leading expert on Rheb, and within the UK, I am the only researcher with an established lab working exclusively on TSC and mTOR at the protein level and who is directly tied in with genetics and clinicians. My follow-up work in the UK revealed that mTOR directly regulated the transcriptional activity of Hypoxic Inducible Factor 1alpha (HIF1alpha), and Signal transducer and activator of transcription 3 (STAT3) and is involved in cancer progression in TSC. Collectively, my research on TSC uncovered that the TSC1 and TSC2 gene products inhibited cell growth through repression of mTOR. This fundamental research was then translated into the clinical setting for the treatment of TSC patients with the use of the mTOR inhibitor, rapamycin. Consequently, the Division of Cancer and Genetics within Cardiff University completed a phase II clinical trial of the safety and efficacy of sirolimus therapy (a rapamycin analogue) for renal angiomyolipomas in patients with TSC. My strong cellular biology research background on TSC and mTOR signalling fits strategically into the current research on TSC within the division. We work closely as a TSC research team with clinicians and geneticists at Cardiff to find cellular mechanisms that can be exploited for potential therapy.

近期论文

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Tee, A.et al. 2016. The role of mTOR signalling in neurogenesis, insights from tuberous sclerosis complex. Seminars in Cell and Developmental Biology 52, pp. 12-20. (10.1016/j.semcdb.2016.01.040) Carroll, B.et al. 2016. Control of TSC2-Rheb signaling axis by arginine regulates mTORC1 activity. eLife 5, article number: e11058. (10.7554/eLife.11058) pdf Upadhyaya, M.et al. 2015. Correlation of copy number changes and gene expression in neurofibromatosis1-associated malignant peripheral nerve sheath tumours. Pediatric Blood and Cancer 62, pp. S152-S152. Zhang, L.et al. 2015. Reversal of pathological features of Graves' orbitopathy by activation of forkhead transcription factors, FOXOs. Journal of Clinical Endocrinology & Metabolism 101(1), pp. 114-122. (10.1210/jc.2015-2932) Rad, E.et al. 2015. STAT3 and HIF1 signaling drives oncogenic cellular phenotypes in malignant peripheral nerve sheath tumors. Molecular Cancer Research 13(7), pp. 1149. (10.1158/1541-7786.MCR-14-0182) pdf Thomas, L.et al. 2015. Evaluation of copy number variation and gene expression in neurofibromatosis type-1-associated malignant peripheral nerve sheath tumours. Human Genomics 9(1), article number: 3. (10.1186/s40246-015-0025-3) pdf Johnson, C.et al. 2015. Endoplasmic reticulum stress and cell death in mTORC1-overactive cells is induced by nelfinavir and enhanced by chloroquine. Molecular Oncology 9(3), pp. 675-688. (10.1016/j.molonc.2014.11.005) pdf Tee, A. 2014. Fundamental for life: mTOR orchestrates developing biological systems. Seminars in Cell & Developmental Biology 36, pp. 66-67. (10.1016/j.semcdb.2014.10.001) Dunlop, E. and Tee, A. 2014. mTOR and autophagy: a dynamic relationship governed by nutrients and energy. Seminars in Cell and Developmental Biology 36, pp. 121-129. (10.1016/j.semcdb.2014.08.006) Zhang, L.et al. 2014. Possible targets for nonimmunosuppressive therapy of Graves' orbitopathy. Journal of Clinical Endocrinology & Metabolism 99(7), pp. E1183-E1190. (10.1210/jc.2013-4182) Yan, M.et al. 2014. The tumor suppressor folliculin regulates AMPK-dependent metabolic transformation. The Journal of Clinical Investigation 124(6), pp. 2640-2650. (10.1172/JCI71749) pdf