Area of research
Molecular Biology · Immunology
Research interest
Research interests include interferon and immune responses, CRISPR and Genetic Engineering, SARS-CoV-2 and COVID-19 Research, and Viral Infections and Immunology Research.
Galectin-9 is a restrictor of infection with multiple enteroviruses.
WSTF nuclear autophagy regulates chronic but not acute inflammation
WSTF nuclear autophagy regulates chronic but not acute inflammation.
PLSCR1 suppresses SARS-CoV-2 infection by downregulating cell surface ACE2.
A genome-wide base-editing screen uncovers a pivotal role of paxillin δ ubiquitination in influenza virus infection.
Circular RNA vaccines against SARS-CoV-2 and emerging variants
Gasdermin E is required for induction of pyroptosis and severe disease during enterovirus 71 infection.
ID2 inhibits innate antiviral immunity by blocking TBK1- and IKKε-induced activation of IRF3.
Nuclear autophagy interactome unveils WSTF as a constitutive nuclear inhibitor of inflammation
SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation.
TRIM26 is a critical host factor for HCV replication and contributes to host tropism.
Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infection
Activation and evasion of type I interferon responses by SARS-CoV-2
Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients
Activation and evasion of type I interferon responses by SARS-CoV-2.
Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients.
Genomic Diversity of Severe Acute Respiratory Syndrome–Coronavirus 2 in Patients With Coronavirus Disease 2019
Genomic Diversity of Severe Acute Respiratory Syndrome-Coronavirus 2 in Patients With Coronavirus Disease 2019.
Overly Exuberant Innate Immune Response to SARS-CoV-2 Infection
Overly Exuberant Innate Immune Response to SARS-CoV-2 Infection
Genome-wide interrogation of gene functions through base editor screens empowered by barcoded sgRNAs
Programmable RNA editing by recruiting endogenous ADAR using engineered RNAs.
Author Correction: Programmable RNA editing by recruiting endogenous ADAR using engineered RNAs.
PASTMUS: mapping functional elements at single amino acid resolution in human cells.
In vivo ways to unveil off-targets.
Leveraging Endogenous ADAR for Programmable Editing on RNA
Cytoplasmic chromatin triggers inflammation in senescence and cancer
The Golgi protein ACBD3 facilitates Enterovirus 71 replication by interacting with 3A
3C Protease of Enterovirus D68 Inhibits Cellular Defense Mediated by Interferon Regulatory Factor 7
Enterovirus 68 3C Protease Cleaves TRIF To Attenuate Antiviral Responses Mediated by Toll-Like Receptor 3