(2019) Nicotinamide riboside augment the aged human skeletal muscle NAD+ metabolome and induces transcriptiomic and anti-inflammatiory signatures. Įlhassan Y, Kluckova K, Fletcher R, Schmidt M, Garten A, Doig C, Cartwright D, Oakey L, Burley C, Jenkinson N, Wilson M, Lucas S, Akerman I, Seabright A, Lai YC, Tennant D, Nightinggale P, Wallis G, Manolopoulos K, Brenner C, Philp A, Lavery G. BioRxiv (Cold Spring Harbor Laboratory) doi. (2019) PINK1-dependent phosphorylation of Serine111 within the SF3 motif of Rab GRPases impairs effector interactions and LRRK2 mediated phosphorylation at Threonine72. Vieweg S, Mulholland K, Brauning B, Kachariya N, Lai YC, Toth R, Sattler M, Groll M, Itzen A, Muqit M. To request meterials please contact Yu-Chiang directly by email: since 2012: Our published research reagents are available to scientific community. 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. Thus, only extending life is not enough and we need to find drugs that delay diseases of old age. However, a longer life for many will mean more years of chronic diseases. 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.īy 2050, the number of people over 60 years old will reach 2 billion worldwide (22% of the population). 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.

The interplay of protein phosphorylation and ubiquitylation in muscle metabolism after exercise.

Identify novel ubiquitin E3 ligases, deubiquitylases (DUBs), and binding proteins in muscle atrophy.

Elucidate how MuRF1 (TRIM63) and MAFbx (FBXO32) contribute to muscle atrophy.

We thus aim to precisely dissect these signalling mechanisms. It is known that the ubiquitin-regulated proteasomal and lysosomal systems are two major pathways responsible for muscle degradation. 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. Currently, exercise is the only known countermeasure to slow this debilitating process, no approved therapeutic is available. Loss of skeletal muscle is a cause of death in patients with cancers and several immune diseases, remarkably preservation of muscle mass increases survival. Skeletal muscle loss is an underappreciated clinical disorder, not only reducing the quality of life but also contributing to morbidity and mortality. The signalling mechanisms of skeletal muscle wasting and the beneficial effect of exercise. To find out more about Yu-Chaing's research group, please visit Lai Lab. 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. Using SILAC-phosphoproteomic approach he identified that several small GTPase Rab proteins are down-stream substrates of PINK1.

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. 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. 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. 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. During his PhD, Yu-Chiang investigate the role of glycogen content and contraction in skeletal muscle glucose metabolism. 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.

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