Jun-Ping Liu graduated with a medical degree (1980) and a Masters degree in Medical Science (1985) from Bethune Medical University, China. He then practiced as a physician at the Peking University Health Science Center. In 1987, Jun-Ping came to Australia to do a PhD at Prince Henry’s Hospital and Monash University. His thesis was on neuroendocrine regulation of pituitary hormone secretion and actions under the supervision of Dr Dennis Engler and Professor John Funder. He obtained his PhD in 1992 and worked as a postdoc with Professor Phillip Robinson at John Hunter Hospital, Newcastle (1992-1994). He was a Senior Scientific Officer at Newcastle Mater Hospital (1995) and an ARC Queen Elizabeth II Fellow at the Baker Medical Research Institute (1996-2000). He was appointed an NHMRC Senior Research Fellow in 1999, and subsequently, a Senior Lecturer (2002) and Associate Professor (2004) at Monash University.
Jun-Ping’s research has been largely on molecular mechanisms of cellular signal transduction in mammalian cell function and malfunction. He showed that the central noradrenergic and neuropeptide Y pathways cause immediate and prolonged hypothalamic-pituitary-adrenal activation, implicating the pseudo-Cushing’s syndrome of endogenous depression and anorexia nervosa. He purified the GTP-binding protein dynamin from rat brain and found that dynamin is phosphorylated by protein kinase C and dephosphorylated by calcineurin, which are coupled to synaptic polarisation and depolarisation. He found that dynamin II mediates secretory vesicle biogenesis from the trans-Golgi membrane of neuroendocrine cells. He recently cloned a novel brain-specific human ATP-binding protein localised at the Golgi apparatus and is currently characterising its function in molecular trafficking and neurodegenerative disease at the molecular and cellular levels in mice.
Working on the mechanisms of cellular maintenance of chromosome ends (telomeres), Jun-Ping showed that protein phosphorylation and dephosphorylation reversibly regulate the enzyme telomerase activity in telomere maintenance in cancer. He identified different gene transcriptional mechanisms that regulate the telomerase gene TERT in telomere remodelling by various transcription factors and repressors in response to hormones, growth factors and cytokines. He found that telomerase maintenance of the telomeres is involved in abnormal vascular cell proliferation in rat genetic hypertension, and that telomerase without its catalytic activity also maintains telomeres in cancer cells. He found that TGF-beta family cytokines induce telomere shortening, tumour cell ageing, and tumour growth inhibition in mice. His current research further investigates different modes of telomere maintenance and remodelling in order to find strategies to treat cancer.