International Centre for Genetic Engineering and Biotechnology
34149 Trieste, Italy
Leeds University, UK, BSc Hons in Microbiology, 1981
Department of Microbiology, Leeds University, UK. Performed PhD studies with Ken Powell on Herpes Simplex Virus proteins and viral replication. 1981-1984
Department of Microbiology, Leeds University, UK, PhD, 1984
Since July 2019- Director-General of the ICGEB, Trieste, Italy
2016-June 2019, Scientific Coordinator, ICGEB
Since 1990, Group Leader of the Tumour Virology Laboratory at ICGEB, Trieste, Italy, during which time the laboratory has become internationally renowned for its work on Human Papillomaviruses and their roles in the development of human malignancy.
1988-1990, independent Research Scientist at the Ludwig Institute for Cancer Research in London, UK, where he continued his studies on the role of Human Papillomavirus oncoproteins in the development of cervical cancer.
1984-1988, Post Doctoral Fellow at the Imperial Cancer Research Fund in London, UK, working with Lionel Crawford on p53 and Human Papillomaviruses.
He is Journal Editor on Journal of Virology, FEBS Journal, Papillomavirus Research, PLoS One, and is on the Editorial Boards of Antiviral Therapy, Virology, Virus Research and Biological Chemistry
Human Papillomaviruses (HPVs) are the causative agents of a number of human tumours, including cervical cancer, which is a major cause of cancer related death in women in many parts of the developing world. The development of HPV-induced malignancies requires the activity of two viral oncoproteins, E6 and E7. Together they act to deregulate a large number of cellular control pathways, primarily to create an environment favourable for viral replication, but which can ultimately give rise to malignancy. A major activity of the laboratory is to understand the molecular basis underlying the activities of E6 and E7 and how this contributes towards the development of cancer. Since E6 and E7 are essential for maintenance of the tumour phenotype, they also represent excellent candidates for therapeutic intervention in HPV-induced disease, and by characterising the functions of important cellular interacting partners, this can help identify novel therapeutic targets. An important aspect of the laboratory’s work is the relevance that it has for understanding the mechanisms of cancer development in general, with many of the insights gained from studying the mechanisms of action of E6 and E7 being relevant for many other types of cancer.
The Tumour Virology Laboratory also has a strong interest in understanding how HPV enters the target cell. Current studies are focused on understanding how a viral capsid protein, L2, directs the incoming viral genome to the nucleus. In particular, we are interested in how this protein recruits the cellular machinery involved in the regulation of endocytic cargo transport, and thereby ensures the correct trafficking of the incoming viral genome. We are also interested in understanding how post-translational modification of the viral capsid proteins contributes towards virus entry, but also regulates virus assembly during a productive virus infection. These studies are intended to shed light on the fundamental aspects governing virus assembly and uptake, but may also provide information on novel means of therapeutic intervention.
The Group makes use of the latest molecular cell biology and biochemical techniques, focusing primarily on the cellular interacting partners of the viral proteins. As has been seen with many other DNA Tumour Virus models, HPV research offers unique insights into the processes affecting diverse and critical aspects of Cell Biology.
2016 Co-organiser 2nd ICGEB Workshop on Human Papillomavirus
2002, 2004, 2006, 2008, 2010, 2012, 2014, 2016 Co-organiser Theoretical and Practical Course on the Molecular Biology of Leishmania
2015 Organised the ICGEB DNA Tumour Virus Meeting
2014 Co-organiser 1st ICGEB Workshop on Human Papillomavirus
2011 Organised the ICGEB DNA Tumour Virus Meeting
2007 Organised the ICGEB DNA Tumour Virus Meeting.
Member of the scientific committee of the International Papillomavirus Workshop.
2003 Organised the ICGEB DNA Tumour Virus Meeting.
1999 Organised the Workshop “p53: Twenty Years On”.
Since 1992, Lecturer on the PhD course in Molecular Genetics of the International School for Advanced Studies (ISAS/SISSA) Trieste, Italy.
Since 1998 13 PhD students have graduated from the laboratory.
Ganti, K., Massimi, P., Manzo-Merino, J., Tomaic, V., Pim, D., Playford, MP., Lizano, M., Roberts, S., Kranjec, C., Doorbar, J., Banks, L. 2016. Interaction of the Human Papillomavirus E6 oncoprotein with sorting nexin 27 modulates endocytic cargo transport pathways. PLoS Path., 12; e1005854 PubMed link
Padash, B. M., Gilbert, M., Thomas, M., Banks, L., Zhang, B., Auld, V.A. 2016. Drosophila model of HPV E6-induced malignancy reveals essential roles for Magi and the insulin receptor. PLoS Path., 12, e1005789 PubMed link
Boon, SS., Tomaic, V., Thomas, M., Roberts, S. and Banks, L. (2015). Cancer-causing human papillomavirus E6 proteins display major differences in the phospho-regulation of their PDZ interactions. J. Virol., 89, 1579-1586.
Tomaic, V. and Banks, L. (2015). Angelman syndrome-associated ubiquitin ligase UBE3A/E6AP mutants interfere with the proteolytic activity of the proteasome. Cell Death Dis. , 6, e1625.
Kranjec, C., Massimi, P. and Banks, L. (2014). Restoration of MAGI-1 expression in human papillomavirus-positive tumor cells induces cell growth arrest and apoptosis. J. Virol., 88, 7155-7169.
Banks, L., Pim, D., Thomas, M. 2012. Human tumour viruses and the deregulation of cell polarity in cancer. Nat Rev Cancer 12, 877-886 doi: 10.1038/nrc3400 PubMed link
Bergant, M., Banks, L. 2013. SNX17 Facilitates Infection with Diverse Papillomavirus Types. J Virol 87, 1270-1273 doi: 10.1128/JVI.01991-12 PubMed link
Boon, S.S., Banks L. 2013. High-risk human papillomavirus e6 oncoproteins interact with 14-3-3ζ in a PDZ binding motif-dependent manner. J Virol 87, 1586-1595 PubMed link
Subbaiah, V.K., Narayan, N., Massimi, P., Banks, L. 2012. Regulation of the DLG tumor suppressor by β-catenin. Int J Cancer 15, doi: 10.1002/ijc.27519 PubMed link
Krishna Subbaiah, V., Massimi, P., Boon, S.S., Myers, M.P., Sharek, L., Garcia-Mata, R., Banks, L. 2012. The invasive capacity of HPV transformed cells requires the hDlg-dependent enhancement of SGEF/RhoG activity. PLoS Pathog 8, e1002543. doi: 10.1371/journal.ppat.1002543 PubMed link
Bergant Marušič, M, Ozbun, M.A., Campos, S.K., Myers, M.P., Banks, L. 2012.Human papillomavirus L2 facilitates viral escape from late endosomes via sorting nexin 17. Traffic. 13, 455-467 doi: 10.1111/j.1600-0854.2011.01320.x. PubMed link
Kranjec, C., Banks, L. 2011. A systematic analysis of human papillomavirus (HPV) E6 PDZ substrates identifies MAGI-1 as a major target of HPV type 16 (HPV-16) and HPV-18 whose loss accompanies disruption of tight junctions. J. Virol. 85, 1757-1764 PubMed link
Tomaic, V., Pim, D., Thomas, M., Massimi, P., Myers, M.P., Banks, L. 2011. Regulation of the human papillomavirus type 18 E6/E6AP ubiquitin ligase complex by the HECT domain-containing protein EDD. J. Virol. 85, 3120-3127 PubMed link
Nagasaka, K., Pim, D., Massimi, P., Thomas, M., Tomaic, V., Subbaiah, V., Kranjec, C., Nakagawa, S., Yano, T., Taketani, Y., Myers, M., Banks, L. 2010. The cell polarity regulator hScrib controls ERK activation through a KIM site-dependent interaction. Oncogene 29, 5311-5321 PubMed link
Gammoh, N., Isaacson, E., Tomaic, V., Jackson, D., Doorbar, J., Banks, L. 2009. Inhibiton of HPV-16 E7 oncogenic activity by HPV-16 E2. Oncogene 28, 2299-2304 PubMed link
Narayan, N., Massimi, P., Banks, L. 2009. CDK phosphorylation of the discs alrge tumour suppressor controls its localisation and stability. J. Cell Sci. 122, 65-74 PubMed link
Pim, D., Tomaic, V., Banks, L. 2009. The human papillomavirus (HPV) E6* proteins from high-risk, mucosal HPVs can direct the degradation of cellular proteins in the absence of full-length E6 protein. J. Virol. 83, 9603-9674 PubMed link
Tomaic, V., Gardiol, D., Massimi, P., Ozbun, M., Myers, M., Banks, L. 2009. Human and primate tumour viruses use PDZ binding as an evolutionarily conserved mechanism of targeting cell polarity regulators. Oncogene 28, 1-8 PubMed link
Thomas, M., Narayan, N., Pim, D., Tomaic, V., Massimi, P., Nagasaka, K., Kranjec, C., Gammoh, N., Banks, L. 2008. Human papillomaviruses, cervical cancer and cell polarity. Oncogene 27, 6876-6877 PubMed link
Tomaic, V., Pim, D., Banks, L. 2009. The stability of the human papillomavirus E6 oncoprotein is E6AP dependent. Virology 393, 7-10 PubMed link
Ainsworth, J., Thomas, M., Banks, L., Coutlee, F., Matlashewski, G. 2008. Comparison of p53 and the PDZ domain containing protein MAGI-3 regulation by the E6 protein from high-risk human papillomaviruses. Virol. J. 5, 67-72
Cavatorta, A., Giri, A., Banks, L., Gardiol, D. 2008. Cloning and functional analysis of the promoter region of the human discs alrge gene. Gene 424, 87-95
Cordano, P., Gillan, V., Bratlie, S., Bouvard, V., Banks, L., Tommasino, M., Campo, M. 2008. The E6E7 oncoproteins of cutaneous human papillomavirus type 38 interfere with the interferon pathway. Virology 377, 408-418
Humbert, P., Banks, L. 2008. On the guardians of polarity and the disorientation of cancer. Oncogene 27, 6876-6877
Massimi, P., Narayan, N., Thomas, M., Gammoh, N., Strand, S., Strand, D., Banks, L. 2008. Regulation of the hDlg/hScrib/Hugl-1 tumour suppressor complex. Exp. Cell Res. 314, 3306-3317 PubMed link
Massimi, P., Shai, A., Lambert, P., Banks, L. 2008. HPV E6 degradation of p53 and PDZ containing substrates in an E6AP null background. Oncogene 27, 1800-1804
Massimi, P., Thomas, M., Bouvard, V., Ruberto, I., Campo, M., Tommasino, M., Banks, L. 2008. Comparative transforming potential of different human papillomaviruses associated with non-melanoma skin cancer. Virology 371, 374-379
Mohr, S., Grandemange, S., Massimi, P., Darai, G., Banks, L., Martinou, J., Zeier, M., Muranyi, W. 2008. Targeting the retinoblastoma protein by MC007L gene product of the molluscum contagiosum virus: detection of a novel virus-cell interaction by a member of the poxviruses. J. Virol. 82, 10625-10633
Thomas, M., Dasgupta, J., Zhang, Y., Chen, X., Banks, L. 2008. Analysis of specificity determinants in the interactions of different HPV E6 proteins with their PDZ domain-containing substrates. Virology 376, 371-378
Thomas, M., Narayan, N., Pim, D., Tomaic, V., Massimi, P., Nagasaka, K., Kranjec, C., Gammoh, N., Banks, L. 2008. Human Papillomaviruses, cervical cancer and cell polarity. Oncogene 27, 7018-7030 PubMed link
Ivanova, S., Repnik, U., Banks, L., Turk, V., Turk, B. 2007. Cellular localization of MAGI-1 caspase cleavage products and their role in apoptosis. Biol Chem. 388, 1195-1198
Zhang, Y., Dasgupta, J., Ma, R., Banks, L., Thomas, M., Chen, X. 2007. Structures of a human papillomavirus (HPV) E6 polypeptide bound to MAGUK proteins: mechanisms of targeting tumor suppressors by a high-risk HPV oncoprotein. J. Virol. 81, 3618-3626 PubMed link
Gammoh, N., Grm, H.S., Massimi, P., Banks, L. 2006. Regulation of human papillomavirus type 16 E7 activity through direct protein interaction with the E2 transcriptional activator. J. Virol. 80, 1787-1797
Gardiol, D., Zacchi, A., Petrera, F., Stanta, G., Banks, L. 2006. Human Discs Large and Scrib are localised at the same regions in colon mucosa and changes in their expression patterns are correlated with loss of tissue architecture during malignant progression. Int. J. Cancer 119, 1285-1290
Massimi, P., Narayan, N., Cuenda, A., Banks, L. 2006. Phosphorylation of the discs large tumour suppressor protein controls its membrane localisation and enhances its susceptibility to HPV E6-induced degradation. Oncogene 25, 4276-4285
Gregorc, U., Ivanova, S., Thomas, M., Turk, V., Banks, L., Turk, B. 2005. hDlg/SAP97, a member of the MAGUK protein family, is a novel caspase target during cell-cell detachment in apoptosis. Biol. Chem. 386, 705-710
Grm, H.S., Massimi, P., Gammoh, N., Banks, L. 2005. Crosstalk between the human papillomavirus E2 transcriptional activator and the E6 oncoprotein. Oncogene 24, 5149-5164
Massimi, P., Banks, L. 2005. Transformation assays for HPV oncoproteins. Methods Mol. Med. 119, 381-395
Pim, D., Massimi, P., Dilworth, S.M., Banks, L. 2005. Activation of the protein kinase B pathway by the HPV-16 E7 oncoprotein occurs through a mechanism involving interaction with PP2A. Oncogene 24, 7830-7838
Thomas, M., Banks, L. 2005. In vitro assays of substrate degradation induced by high-risk HPV E6 oncoproteins. Methods Mol. Med. 119, 411-417
Thomas, M., Massimi, P., Navarro, C., Borg, J.P., Banks, L. 2005. The hScrib/Dlg apico-basal control complex is differentially targeted by HPV-16 and HPV-18 E6 proteins. Oncogene 24, 6222-6230
Thomas, M., Pim, D., Banks, L. 2005. The role of the HPV E6 oncoprotein in malignant progression. In: Papillomavirus Research: From natural history to vaccines and beyond. Ed. M. S. Campo, Calster Academic Press
Banks, L., Pim, D., Thomas, M. 2003. Viruses and the 26S proteasome: hacking into destruction. Trends Biochem. Sci. 28, 452-459
Mantovani, F., Banks, L. 2003. Regulation of the discs large tumour suppressor by a phosphorylation-dependent interaction with the BTrCP ubiquitin ligase receptor. J. Biol. Chem. 278, 42477-42486