Cheung Ching For, Peter


Cheung Ching For, Peter

Cheung Ching For, Peter
Assistant Professor

Office: 03n-09
Telephone: 6316 2849



  • BSc - Biochemistry, Cardiff University, UK
  • MSc - Toxicology, Imperial College, University of London, UK
  • PhD - Biochemistry, Imperial College, University of London, UK

Professional Experience

  • Postdoctoral Fellow, MRC Protein Phosphorylation Unit, University of Dundee, UK

Research Interest

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.

In vivo, TAK1 exists as two distinct heterotrimeric forms. One consists of TAK1-TAB1-TAB2 and the other TAK1-TAB1-TAB3. It is known that TAB1 is required for TAK1 activity, and that TAB2 or TAB3 may act as a link with upstream regulators. My recent work has shown that p38α is involved in the down-regulation of TAK1 activity and the identification of TAB3 as a new binding partner of TAK1.