- Molecular virology
- Innate antiviral response
- Transcriptional regulation
My current research focuses primarily on the molecular basis of biological as well as virological processes. Various molecular approaches have been used to conduct basic research in molecular biology and virology.
On one hand, I have been working with many different viruses including influenza A virus, SARS-CoV-2, SARS-CoV, MERS-CoV, measles virus, HBV, EBV, HTLV-1, and zika virus. We aim to dissect the regulatory mechanism of innate antiviral response and viral-host interactions. Over the years, we have identified and characterized novel cellular and viral regulatory factors that govern antiviral response. Particularly, cellular machinery to sense viral nucleic acids as well as features of viral nucleic acids being sensed have been dissected. Our more recent study demonstrates dual anti-influenza A virus activity of PACT mediated through coactivation of RIG-I and suppression of viral polymerase (Chan et al., 2018). We strive to advance our current understanding of viral-host interactions. Our findings might also reveal novel strategies for developing antiviral and immunomodulatory agents.
On the other hand, we have been studying liver-enriched transcription factor CREB-H for more than a decade. CREB-H is an ER-bound transcription factor which has been shown to regulate lipid metabolism, gluconeogenesis, iron homeostasis, acute phase response, ER stress and cell growth. Its role as a central regulator of energy homeostasis governing lipid and glucose metabolism has emerged. Previously, we have reported that N-linked glycosylation is required for optimal proteolytic activation of CREB-H (Chan et al., 2010). Recently, we defined a regulatory step in the turnover of CREB-H ΔTC (Cheng et al., 2016). We found that CREB-H ΔTC physically interacts with β-TrCP which elevates polyubiquitination and hence destabilizes CREB-H ΔTC. An evolutionarily conserved degron in CREB-H ΔTC was also identified and characterized. Currently, we have been working on additional CREB-H novel targets for better understanding of its biological roles, particularly in inflammatory responses. The new knowledge gained might instruct future development of therapeutics for various liver diseases such as hepatic fibrosis and HCC.
- Cheung, P.H.H., Lee, T.W.T., Kew, C., Chen, H., Yuen, K.Y., Chan, C.P.*, and Jin, D.Y.* (2020). Virus subtype-specific suppression of MAVS aggregation and activation by PB1-F2 protein of influenza A (H7N9) virus. PLOS Pathogens. (In press). DOI: 10.1371/journal.ppat.1008611. (*Co-Corresponding Authors)
- Cheung, P.H.H., Ye, Z.W., Lee, T.W.T., Chen, H., Chan, C.P.*, and Jin, D.Y.* (2020). PB1-F2 protein of highly pathogenic influenza A (H7N9) virus selectively suppresses RNA-induced NLRP3 inflammasome activation through inhibition of MAVS-NLRP3 interaction. Journal of Leukocyte Biology. (In press). DOI: 10.1002/JLB.4AB0420-694R. (*Co-Corresponding Authors)
- Siu, K.L., Yuen, K.S., Castaño-Rodriguez, C., Ye, Z.W., Yeung, M.L., Fung, S.Y., Yuan, S., Chan, C.P., Yuen, K.Y., Enjuanes, L., and Jin, D.Y. (2019). Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC. FASEB Journal. 33(8):8865-77.
- Chan, C.P.*, Yuen, C.K.*, Cheung, P.H., Fung, S.Y., Lui, P.Y., Chen, H.L., Kok, K.H., Jin, D.Y. (2018). Antiviral activity of double-stranded RNA-binding protein PACT against influenza A virus mediated through suppression of viral RNA polymerase. FASEB Journal. 32(8):4380-4393. (*Equal First Authors)
- Wang, P.H., Fung, S.Y., Gao, W.W., Deng, J.J., Cheng, Y., Chaudhary, V., Yuen, K.S., Ho, T.H., Chan, Ching-P., Zhang, Y., Kok, K.H., Yang, W., Chan, C.P., and Jin, D.Y. (2018). A novel transcript isoform of STING that sequesters cGAMP and dominantly inhibits innate nucleic acid sensing. Nucleic Acids Research. 46(8):4054-4071.
- Wang, P.H., Ye, Z.W., Deng, J.J., Siu, K.L., Gao, W.W., Chaudhary, V., Cheng, Y., Fung, S.Y., Yuen, K.S., Ho, T.H., Chan, Ching-P., Zhang, Y., Kok, K.H., Yang, W., Chan, C.P., and Jin, D.Y. (2018). Inhibition of AIM2 inflammasome activation by a novel transcript isoform of IFI16. EMBO Reports. 19(10). e45737.
- Gao, W.W., Tang, H.M.V., Cheng, Y., Chan, Ching-P., Chan, C.P.*, and Jin, D.Y.* (2018). Suppression of gluconeogenic gene transcription by SIK1-induced ubiquitination and degradation of CRTC1. Biochim Biophys Acta - Gene Regulatory Mechanisms. 1861(3):211-223. (*Co-Corresponding Authors)
- Cheng, Y., Gao, W.W., Tang, H.M.V., Deng, J.J., Wong, C.M., Chan, C.P.*, and Jin, D.Y.* (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. Scientific Reports. 6:23938. doi:10.1038/srep23938 (*Co-Corresponding Authors)
- Tang, H.M.V.*, Gao, W.W.*, Chan, C.P.*, Cheng, Y., Deng, J.J., Yuen, K.S., Iha, H., and Jin, D.Y. (2015). SIRT1 Suppresses Human T-Cell Leukemia Virus Type 1 Transcription. Journal of Virology. 89(16):8623-31. (*Equal First Authors)
- Tang, H.M.V.*, Gao, W.W.*, Chan, C.P.*, Cheng, Y., Chaudhary, V., Deng, J.J., Yuen, K.S., Wong, C.M., Ng, I.O.L., Kok, K.H., Zhou, J., and Jin, D.Y. (2014). Requirement of CRTC1 coactivator for hepatitis B virus transcription. Nucleic Acid Research. 42(20):12455-12468. (*Equal First Authors)
- Health and Medical Research Fund (HMRF), 2020 (Principal Applicant)
- GD-NSF (General Programme), 2019 (Principal Investigator)
- Collaborative Research Fund (CRF), 2016 (Co-principal Investigator)
- Health and Medical Research Fund (HMRF), 2015 (Principal Applicant)
- NSFC (Science Fund for Young Scholars), 2015 (Principal Investigator)
- General Research Fund (GRF), 2018 (Co-Investigator)
- General Research Fund (GRF), 2018 (Co-Investigator)
- Health and Medical Research Fund (HMRF), 2018 (Co-Applicant)
- Health and Medical Research Fund (HMRF), 2017 (Co-Applicant)
- Health and Medical Research Fund (HMRF), 2016 (Co-Applicant)
- Member, The American Society for Cell Biology (ASCB)
- Member, The Society of Chinese Bioscientists in America (SCBA)
Last update: July 2, 2020