Area of research
Immunology · Infectious Diseases
Research interest
Research interests include interferon and immune responses, SARS-CoV-2 and COVID-19 Research, Invertebrate Immune Response Mechanisms, and COVID-19 Clinical Research Studies.
Anti-renal amyloidosis potential of rosemary extract: A multidimensional mechanistic study
Coronavirus envelope protein activates TMED10-mediated unconventional secretion of inflammatory factors.
SARS-CoV-2 Phylointeractomics Reveal Functional Evolution of Its Variants Across Susceptible Human Organs
A comprehensive SARS-CoV-2-human protein-protein interactome reveals COVID-19 pathobiology and potential host therapeutic targets.
SARS‐CoV‐2 NSP7 inhibits type I and III IFN production by targeting the RIG‐I/MDA5, TRIF, and STING signaling pathways
SARS-CoV-2 Nsp8 suppresses MDA5 antiviral immune responses by impairing TRIM4-mediated K63-linked polyubiquitination
SARS-CoV-2 NSP7 inhibits type I and III IFN production by targeting the RIG-I/MDA5, TRIF, and STING signaling pathways.
SARS-CoV-2 NSP8 suppresses type I and III IFN responses by modulating the RIG-I/MDA5, TRIF, and STING signaling pathways.
A comprehensive SARS-CoV-2–human protein–protein interactome reveals COVID-19 pathobiology and potential host therapeutic targets
SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules
SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules.
SARS‐CoV‐2 ORF10 antagonizes STING‐dependent interferon activation and autophagy
SARS-CoV-2 membrane protein causes the mitochondrial apoptosis and pulmonary edema via targeting BOK
SARS-CoV-2 ORF10 antagonizes STING-dependent interferon activation and autophagy.
SARS-CoV-2 membrane protein causes the mitochondrial apoptosis and pulmonary edema via targeting BOK.
SARS-CoV-2 ORF3a induces RETREG1/FAM134B-dependent reticulophagy and triggers sequential ER stress and inflammatory responses during SARS-CoV-2 infection
GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia
SARS-CoV-2 ORF3a induces RETREG1/FAM134B-dependent reticulophagy and triggers sequential ER stress and inflammatory responses during SARS-CoV-2 infection.
GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia.
A C-terminal glutamine recognition mechanism revealed by E3 ligase TRIM7 structures.
An antibody-based proximity labeling map reveals mechanisms of SARS-CoV-2 inhibition of antiviral immunity.
SARS-CoV-2 N protein potentiates host NPM1-snoRNA translation machinery to enhance viral replication.
Inhibition of SARS-CoV-2 replication by zinc gluconate in combination with hinokitiol.
Antibiotic-Induced Primary Biles Inhibit SARS-CoV-2 Endoribonuclease Nsp15 Activity in Mouse Gut
Antibiotic-Induced Primary Biles Inhibit SARS-CoV-2 Endoribonuclease Nsp15 Activity in Mouse Gut.
ORF3a of the COVID-19 virus SARS-CoV-2 blocks HOPS complex-mediated assembly of the SNARE complex required for autolysosome formation.
SARS‐CoV‐2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG‐I/MDA‐5–MAVS, TLR3–TRIF, and cGAS–STING signaling pathways
SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING signaling pathways.
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling.