Dr Yu-Chiang Lai PhD

• PhD in Exercise Physiology & Metabolism, Norwegian School of Sport Science, Oslo, Norway (2010)
• MSc in Sport Science, University of Taipei, Taiwan (2005)

Yu-Chiang graduated with an MSc in Sport Science from the University of Taipei, Taiwan and completed his PhD in Exercise Physiology at the Norwegian School of Sport Sciences and National Institute of Occupational Health, Oslo, Norway under the supervision of Professor Jorgen Jensen. During his PhD, Yu-Chiang investigate the role of glycogen content and contraction in skeletal muscle glucose metabolism. 

Yu-Chiang was awarded the Christian de Duve Institute Fellowship in 2010 and joined Professor Mark Rider’s laboratory at the de Duve Institute (note: Professor Christian de Duve received the Nobel Prize in Medicine or Physiology in 1974), Université Catholique de Louvain, Brussels, Belgium. From 2011, his work was funded by FNRS (The National Fund for Scientific Research for French community in Belgium) to study the energy sensing AMPK signaling pathways in the regulation of cellular metabolism and function. He worked closely with AstraZeneca, a global pharmaceutical company, to develop muscle AMPK activators and also identified PDE4B a new AMPK substrate in hepatocytes that counteracts glucagon-stimulated cyclic-AMP and glucose productions.

In 2014, Yu-Chiang Joined Professor Miratul Muqit’s laboratory as a senior postdoctoral researcher at the MRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, to investigate PINK1 and Parkin signalling pathway in Parkinson’s disease and mitophagy. Using SILAC-phosphoproteomic approach he identified that several small GTPase Rab proteins are down-stream substrates of PINK1.

In 2018, Yu-Chiang was awarded a Birmingham Fellowship to establish his own laboratory aiming to understand the signaling mechanisms of muscle atrophy and exercise.

If you are interested in joining Yu-Chiang’s research group, please contact him directly through email with a brief motivation letter and CV.

Email: y.lai.1@bham.ac.uk

To find out more about Yu-Chaing's research group, please visit Lai Lab.

The signalling mechanisms of skeletal muscle wasting and the beneficial effect of exercise.

Skeletal muscle loss is an underappreciated clinical disorder, not only reducing the quality of life but also contributing to morbidity and mortality. Loss of skeletal muscle is a cause of death in patients with cancers and several immune diseases, remarkably preservation of muscle mass increases survival. Currently, exercise is the only known countermeasure to slow this debilitating process, no approved therapeutic is available.

The loss of muscle mass and strength primarily results from excessive protein degradation, often accompanied by reduced protein synthesis, resulting in a negative net balance. It is known that the ubiquitin-regulated proteasomal and lysosomal systems are two major pathways responsible for muscle degradation. We thus aim to precisely dissect these signalling mechanisms.

Current projects are

1. Elucidate how MuRF1 (TRIM63) and MAFbx (FBXO32) contribute to muscle atrophy
2. Identify novel ubiquitin E3 ligases, deubiquitylases (DUBs), and binding proteins in muscle atrophy
3. The interplay of protein phosphorylation and ubiquitylation in muscle metabolism after exercise

We tackle these questions using a range of state-of-the-art techniques, including molecular & cellular engineering (such as CRISPR/Cas9 genetic editing), biochemistry, chemical biology, mass spectrometry and mouse genetics. Importantly, we are also exploring the physiological role of the ubiquitin system in skeletal muscle and therefore translating basic science to clinical research by employing human samples that are well established at the School of SportExR (University of Birmingham) and the MRC-ARUK Centre of Musculoskeletal and Ageing Research, joint with the University of Nottingham.

By 2050, the number of people over 60 years old will reach 2 billion worldwide (22% of the population). However, a longer life for many will mean more years of chronic diseases. Thus, only extending life is not enough and we need to find drugs that delay diseases of old age. A further aim of my research is therefore to identify which components of exercise-mediated signalling pathways are the most attractive drug target for the treatment of muscle loss and other age-related diseases.

Our published research reagents are available to scientific community. To request meterials please contact Yu-Chiang directly by email: y.lai.1@bham.ac.uk.