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Peter Cheung's Lab
DESCRIPTION OF LAB RESEARCH WORK
My research concerns the identification and mapping of signaling pathways involved in inflammation. Currently, we are investigating the mechanism of activation of TAK1, a mitogen activated protein kinase kinase kinase (MAPKKK). TAK1 is activated by pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor-α (TNF-α), and also by bacterial lipopolysaccharides (LPS). Engagement of these three stimuli with their receptors leads to the activation of the inflammatory response via the JNK, p38α and NFκB pathways which all lie downstream of TAK1. However, dysregulation of these pathways can lead to chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis and asthma. As TAK1 is a key component in transducing inflammatory signals, inhibition of TAK1 by therapeutic means may be attractive as treatment for these diseases.
My research concerns the identification and mapping of signaling pathways involved in inflammation. Currently, we are investigating the mechanism of activation of TAK1, a mitogen activated protein kinase kinase kinase (MAPKKK). TAK1 is activated by pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor-α (TNF-α), and also by bacterial lipopolysaccharides (LPS). Engagement of these three stimuli with their receptors leads to the activation of the inflammatory response via the JNK, p38α and NFκB pathways which all lie downstream of TAK1. However, dysregulation of these pathways can lead to chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis and asthma. As TAK1 is a key component in transducing inflammatory signals, inhibition of TAK1 by therapeutic means may be attractive as treatment for these diseases.
 | LEAD PI Cheung Ching For Peter Senior Lecturer Assistant Chair (Exchange and SkillsFuture) Email: [email protected] Phone:(65) 6316 2849 Office: SBS-03N-09 |
- TAK1
- Pellino1
- Dai L, Lin J, Binte Said A, Yau YH, Geifman Shochat S, Ruiz-Carillo D, Sun K, Chandrasekaran R, Sze SK, Lescar J and Cheung PCF. (2019). Pellino1 specifically binds to phospho-Thr18 of p53 and is recruited to sites of DNA damage. BBRC. Apr 12. pii: S0006-291X(19)30484-X. doi: 10.1016/j.bbrc.2019.03.095.
- Ruiz-Carrillo D, Lin J, El Sahili A, Wei M, Sze SK, Cheung PCF, Doerig C, Lescar J. (2018). The protein kinase CK2 catalytic domain from Plasmodium falciparum: crystal structure, tyrosine kinase activity and inhibition. Sci Rep. 2018 May 9;8(1):7365.
- Liu, X., Dai, L., Chan, A. T., Xi, J. and Cheung, P. C. F. (2012). TAK1ng the road from immunity to DNA damage and beyond. IUBMB Life. Review. Oct;64(10):825-34. irology. 521:20-32. (Cover page)
- Karine Enesa, Alban Ordureau, Hilary Smith, David Barford, Peter CF Cheung, Simon Arthur and Philip Cohen (2012). Defective production of type 1 interferons in mice expressing an E3-ligase deficient mutant of Pellino1. J. Biol. Chem. 287 (41):34825-35.
- Richard Sutejo, Dawn SY Yeo, Myint Zu Myaing, Debbie Ko, Hui Chen, Jiajia Xi, Peter CF Cheung, Boon Huan Tan and Richard J Sugrue. (2012). The activation of interferon type 1 and 3 signaling pathways in low pathogenic avian influenza virus infected lung epithelial cells. Accepted PLos One. (Impact factor 4.41)
- Goh ET, Arthur JS, Cheung PCF, Akira S, Toth R, Cohen P. (2011). Identification of the protein kinases that activate the E3 ubiquitin ligase Pellino 1 in the innate immune system. Biochem J. 441 (1):339-46
- Smith H, Liu X, Dai L, Chan AT, Xi J, Seh CC, Lescar J, Ruedl C, Cohen P. and Cheung PCF. (2011). The role of TBK1 and IKK in the expression
- Lam CRI, Tan MJ, Tan SH, Tang MBY, Cheung PCF and Tan NS (2011). TAK1 regulates SCF expression to modulate PKB activity that protects keratinocytes from ROS-induced apoptosis. Cell Death and Differentiation. 2011 Jan 14.
- Scholz R, Sidler CL, Thali RF, Winssinger N, Cheung PCF and Neumann D (2010). Sequential TAB1-induced TAK1 autoactivation revealed by bacterial expression of TAK1 complexes and probing with AMPK as a substrate. J. Biol. Chem. 285, 25753–25766