About the National University of Singapore

About NUSA leading global university centred in Asia, NUS is Singapore's flagship university, offering a global approach to education and research with a focus on Asian perspectives and expertise.

About the Mechanobiology Institute, National University of Singapore

About MBIOne of four Research Centres of Excellence at NUS, MBI is working to identify, measure and describe how the forces for motility and morphogenesis are expressed at the molecular, cellular and tissue level.
Marius Sudol 2017-05-03T10:53:59+00:00
Marius SUDOL

Marius SUDOL

Co-Principal Investigator, Mechanobiology Institute, National University of Singapore

mbims@nus.edu.sgphsms@nus.edu.sg
+65 6601 1557 ext 11557
Level 10 T-Lab
National University of Singapore
5A Engineering Drive 1
Singapore 117411

Curriculum Vitae

Research Program
The Cell-Matrix and Cell-Cell Mechanotransduction Group

Affiliations
Associate Professor, Yong Loo Lin School of Medicine, Department of Physiology, NUS, Institute for Molecular and Cell Biology (IMCB, AStar)

Marius Sudol

Co-Principal Investigator

Research Areas

  • Investigations into physiological and molecular mechanisms of the Golabi-Ito-Hall syndrome, which phenocopies severe autism, using transgenic animal models of the syndrome
  • Investigations into the role of tight junctions proteins such as ZO2 and ZO1 in the regulation of the Hippo-YAP tumor suppressor pathway using cell and animal models
  • Investigations of new signaling modalities that inhibit YAP oncogene and could be translated into cancer drug discovery
  • Investigations of a cross talk between WW domain-containing proteins that regulate muscle homeostasis and the Hippo-YAP pathway that controls differentiation and stem cell biology
  • Investigations into the dominant role of Hippo-YAP tumor suppressor pathway in liver regeneration

Research Interests

Among Prof Sudol’s most significant achievements to date are the identification of a modular protein domain, known as the WW domain, and the characterization of its cognate ligands. In 2004, together with a research team at AxCell-Cytogen company, Marius Sudol reported the first comprehensive protein interaction map for a human modular domain. Today, the WW domain is known to mediate critical signals in tumor suppressor networks, including the Hippo signaling pathway. More importantly, syndromes such as the Golabi-Ito-Hall syndrome of intellectual disability and Liddle syndrome of hypertension are caused by loss-of-function point mutations in the WW domain or its cognate ligands.

Biography

The research conducted in Marius Sudol’s laboratory and those of his collaborators over the past two decades has directly contributed to a systems biology level understanding of signaling networks from the perspective of modular protein domains. As a co-founder and co-leader of the Protein Modules Consortium, he advocates systems biology approaches and synthetic biology strategies in designing therapeutic interventions based on the knowledge of the structure and function of protein modules.

Over the course of his scientific career spanning more than three decades, Marius Sudol has authored 130 publications, including original research articles and invited reviews in refereed journals as well as numerous book chapters. His current work focuses on the role of WW domain-containing proteins in the Hippo tumor suppressor network and Golabi-Ito-Hall syndrome of intellectual disability.

Education

PhD California Institute of Technology

Recent Publications

  1. Qiao Y, Chen J, Lim YB, Finch-Edmondson ML, Seshachalam VP, Qin L, Jiang T, Low BC, Singh H, Lim CT, and Sudol M. YAP Regulates Actin Dynamics through ARHGAP29 and Promotes Metastasis. Cell Rep 2017; 19(8):1495-1502. [PMID: 28538170]
  2. Finch-Edmondson M, and Sudol M. Framework to function: mechanosensitive regulators of gene transcription. Cell. Mol. Biol. Lett. 2016; 21:28. [PMID: 28536630]
  3. Passaniti A, Brusgard JL, Qiao Y, Sudol M, and Finch-Edmondson M. Roles of RUNX in Hippo Pathway Signaling. Adv. Exp. Med. Biol. 2017; 962:435-448. [PMID: 28299672]
  4. Liang J, Sagum CA, Bedford MT, Sidhu SS, Sudol M, Han Z, and Harty RN. Chaperone-Mediated Autophagy Protein BAG3 Negatively Regulates Ebola and Marburg VP40-Mediated Egress. PLoS Pathog. 2017; 13(1):e1006132. [PMID: 28076420]
  5. Espejo AB, Gao G, Black K, Gayatri S, Veland N, Kim J, Chen T, Sudol M, Walker C, and Bedford MT. PRMT5 C-terminal Phosphorylation Modulates a 14-3-3/PDZ Interaction Switch. J. Biol. Chem. 2016;. [PMID: 28031468]
  6. Lim SK, Lu SY, Kang S, Tan HJ, Li Z, Adrian Wee ZN, Guan JS, Reddy Chichili VP, Sivaraman J, Putti T, Thike AA, Tan PH, Sudol M, Virshup DM, Chan SW, Hong W, and Lim YP. Wnt Signaling Promotes Breast Cancer by Blocking ITCH-Mediated Degradation of YAP/TAZ Transcriptional Coactivator WBP2. Cancer Res. 2016; 76(21):6278-6289. [PMID: 27578003]
  7. Pucheta-Martinez E, D'Amelio N, Lelli M, Martinez-Torrecuadrada JL, Sudol M, Saladino G, and Gervasio FL. Changes in the folding landscape of the WW domain provide a molecular mechanism for an inherited genetic syndrome. Sci Rep 2016; 6:30293. [PMID: 27456546]
  8. Li Y, Guo J, Shen H, Li J, Yang N, Frangou C, Wilson KE, Zhang Y, Mussell AL, Sudol M, Farooq A, Qu J, and Zhang J. Phosphorylation of Tyr188 in the WW domain of YAP1 plays an essential role in YAP1-induced cellular transformation. Cell Cycle 2016;. [PMID: 27428284]
  9. Finch-Edmondson ML, Strauss RP, Passman AM, Sudol M, Yeoh GC, and Callus BA. TAZ Protein Accumulation Is Negatively Regulated by YAP Abundance in Mammalian Cells. J. Biol. Chem. 2015; 290(46):27928-38. [PMID: 26432639]
  10. Qiao Y, Lin SJ, Chen Y, Voon DC, Zhu F, Chuang LSH, Wang T, Tan P, Lee SC, Yeoh KG, Sudol M, and Ito Y. RUNX3 is a novel negative regulator of oncogenic TEAD-YAP complex in gastric cancer. Oncogene 2015; 35(20):2664-74. [PMID: 26364597]