Academic Profile

Dr. Tan Suet Mien obtained his B.Sc.(Hons, first class)(1996) and M.Sc. (1998) from the National University of Singapore. He obtained his D.Phil. (2001) from the University of Oxford, UK. He joined the School of Biological Sciences (NTU) in 2001 as Assistant Professor. As a pioneer member of the newly established school, he was involved in curriculum planning, time-tabling, student recruitment apart from setting up his research lab. He served as Sub-Dean (Academic) from 2005-2006, Assistant Chair (Academic) from 2006-2008, and Associate Chair (Academic) from Jul 2011- Jul 2014. He also served as a senator of the NTU Academic Council (2014-2017). He is a recipient of the Nanyang Award for Excellence in Teaching (2006) and the Singapore Public Administration Medal (Bronze, 2013). He currently serves on the NTU Institutional Review Board and Institutional Biosafety Committee.
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Assoc Prof Tan Suet Mien
Associate Professor, School of Biological Sciences

My research group has a long-standing interest in understanding the molecular mechanisms of cell adhesion and migration underpinning normal and pathological conditions, including inflammation and cancer. We focus on two families of molecules – integrins and kindlins. Integrins are heterodimeric transmembrane proteins that mediate cell-cell, cell-extracellular matrix, and cell-virus interactions. Integrin ligand-binding is regulated by its conformational change that is dependent on the interactions between its cytoplasmic domain and cytosolic proteins. These cytosolic proteins can either be positive or negative regulators of integrin function. Currently, my research group and in collaboration with others seek to define the molecular basis of cross-talks between these regulators, and how they modulate integrin ligand-binding, signaling and cytoskeletal re-modelling under normal and pathological conditions, such as chronic inflammation and cancer metastasis.

Kindlins are a small family of FERM-domain-containing cytoplasmic proteins. Three kindlin paralogs have been identified with dissimilar tissue expression profiles. Over the last few years, kindlins emerged as key regulators of integrin activation and signaling. The importance of kindlins is underscored by diseases Kindler syndrome, leukocyte adhesion deficiency III, and cancer. In addition to integrin-affinity regulation, our research group and others have shown that kindlins promote integrin clustering, which strengthens cell-ECM and cell-cell adhesion. There is also gaining evidence that kindlins are involved in cellular signaling conduits that are independent of integrins. We are investigating the roles of kindlins in these pathways in the context of cancer progression.
  • Mechanistic insights into kindlin-3 regulation and their roles in leukemia (MOH-OFIRG18nov-0002)

  • Structural analyses of interactions between kindlin 3 with its binding partners RACK1 and IGF2BP1
  • Chatterjee D, D’Souza A, Zhang Y, Bin W, Tan SM, and Bhattacharjya S. (2018). Interaction analyses of 14-3-3ζ, Dok1, and phosphorylated integrin β cytoplasmic tails reveal a bi-molecular switch in integrin regulation. Journal of Molecular Biology, 430, 4419-4430.

  • Chatterjee D, Lewis Lu ZP, Tan SM and Bhattacharya S. (2018). NMR Structure, Dynamics and Interactions of the Integrin β2 Cytoplasmic Tail with Filamin Domain IgFLNa21. Scientific Reports, 8, 5490.

  • Guan SY, Chng CP, Ong LT, Tan HF, Alex Law SK and Tan SM. (2017). The binding interface of kindlin-2 and ILK involves Asp344/Asp352/Thr356 in kindlin-2 and Arg243/Arg334 in ILK. FEBS Letters, 592, 112-121.

  • Qu J, Ero R, Feng C, Ong LT, Tan HF, Lee HS, Ismail MH, Bu WT, Nama S, Sampath P, Gao YG, and Tan SM. (2015). Kindlin-3 interacts with the ribosome and regulates c-Myc expression required for proliferation of chronic myeloid leukemia cells. Scientific Reports, 5, 18491.

  • Li JL, Lim CH, Tay FW, Goh CC, Devi S, Malleret B, Lee B, Bakocevic N, Chong SZ, Evrard M, Tanizaki H, Lim HY, Russell B, Renia L, Zolezzi F, Poidinger M, Angeli V, John AL, Harris JE, Tey HL, Tan SM, Kabashima K, Weninger W, Larbi A, and Ng LG. (2015). Neutrophils self-regulate immune complex-mediated cutaneous inflammation through CXCL2.. The Journal of Investigative Dermatology, in press.