Shu Li

ORCID: 0000-0002-0007-5198
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About
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Research Areas
  • interferon and immune responses
  • Immune Response and Inflammation
  • NF-κB Signaling Pathways
  • Viral Infections and Vectors
  • Cytokine Signaling Pathways and Interactions
  • RNA regulation and disease
  • Immune Cell Function and Interaction
  • Mosquito-borne diseases and control
  • Ubiquitin and proteasome pathways
  • RNA Research and Splicing
  • Drug Transport and Resistance Mechanisms
  • Nanoparticle-Based Drug Delivery
  • Viral Infections and Immunology Research
  • HIV Research and Treatment
  • IL-33, ST2, and ILC Pathways
  • Immunotherapy and Immune Responses
  • Autophagy in Disease and Therapy
  • Cancer-related Molecular Pathways
  • Animal Disease Management and Epidemiology
  • Sirtuins and Resveratrol in Medicine
  • Hemostasis and retained surgical items
  • Antimicrobial Peptides and Activities
  • Endoplasmic Reticulum Stress and Disease
  • Immune cells in cancer
  • Hepatitis C virus research

Hubei University of Science and Technology
2024-2025

Wuhan University
2014-2024

Chinese Academy of Medical Sciences & Peking Union Medical College
2021-2024

Zhongnan Hospital of Wuhan University
2018-2024

Second Affiliated Hospital of Zhejiang University
2022-2024

Medical Research Institute
2021-2023

Academia Sinica
2022-2023

Frontier Science Foundation
2021-2023

Academy of Medical Sciences
2021-2023

Chinese PLA General Hospital
2023

The programmed cell death 1 (PD-1) immune checkpoint of co-inhibitory signaling plays crucial roles in controlling the magnitude and duration T activation to limit tissue damage maintain self-tolerance. Cancer cells hijack pathway escape surveillance by overexpressing PD-1 ligand PD-L1. Immune inhibitors, such as blocking antibody have been approved for tumor immunotherapy. However, not all patients can benefit from monotherapy. Combination immunotherapy based on axis blockade substantially...

10.1016/j.cellin.2024.100146 article EN cc-by-nc-nd Cell Insight 2024-02-23

Pluronic block copolymer P85 was shown to inhibit the P-glycoprotein (Pgp) drug efflux system and increase permeability of a broad spectrum drugs in blood-brain barrier (BBB). However, there is an entire series Pluronics varying lengths propylene oxide ethylene overall lipophilicity. This study identifies those structural characteristics required for maximal impact on transporter activity bovine brain microvessel endothelial cells (BBMECs). Using wide range copolymers, differing...

10.1124/jpet.102.043307 article EN Journal of Pharmacology and Experimental Therapeutics 2003-01-22

Ubiquitination and deubiquitination have emerged as critical post-translational regulatory mechanisms for activation or attenuation of the virus-triggered type I interferon (IFN) 2The abbreviations used are: IFNinterferonTLRToll-like receptorVSVvesicular stomatitis virusRNAiRNA interferenceSeVSendai virus.2The virus. induction pathways. In this study, we identified two deubiquitinating enzymes, OTUB1 OTUB2, negative regulators IFN induction. Overexpression OTUB2 inhibited virus-induced IRF3...

10.1074/jbc.m109.074971 article EN cc-by Journal of Biological Chemistry 2009-12-08

Cyclic GMP-AMP synthase (cGAS) senses double-strand (ds) DNA in the cytosol and then catalyzes synthesis of second messenger cGAMP, which activates adaptor MITA/STING to initiate innate antiviral response. How cGAS activity is regulated remains enigmatic. Here, we identify ZCCHC3, a CCHC-type zinc-finger protein, as positive regulator cytosolic dsDNA- virus-triggered signaling. We show that ZCCHC3-deficiency inhibits induction downstream effector genes, ZCCHC3-deficient mice are more...

10.1038/s41467-018-05559-w article EN cc-by Nature Communications 2018-08-16

Significance IL-33R mediates local inflammatory responses and plays crucial roles in the pathogenesis of immune diseases. In this study, we identified USP38, which negatively regulates IL-33-triggered signaling by mediating K27-linked deubiquitination at K511 its autophagic degradation. USP38 deficiency aggravates IL-33–induced lung response bleomycin-induced pulmonary fibrosis. We further show that E3 ubiquitin ligase TRAF6 catalyzes polyubiquitination K511, inhibits IL-33–mediated...

10.1073/pnas.2116279119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-03-01

The problem of antibiotic abuse and drug resistance is becoming increasingly serious. In recent years, polydopamine (PDA) nanoparticles have been recognized as a potential antimicrobial material for photothermal therapy (PTT) due to their excellent conversion efficiency unique ability. PDA capable rapidly converting light energy into heat under near-infrared (NIR) irradiation kill bacteria efficiently. order solve the PDA's tendency aggregate precipitate, this study improved its stability by...

10.3390/polym17020162 article EN Polymers 2025-01-10

Abstract Abdominal aortic aneurysm (AAA) is the most common true worldwide, and recent studies suggest that dendritic cells (DCs) play a key role in its development, though specific subtypes underlying mechanisms remain unclear. In this study, of interferon regulatory factor 8 (IRF8) AAA investigated by focusing on effect differentiation DC precursors into conventional type 1 (cDC1s). It found significant infiltration HLA‐DR + IRF8 human tissue samples. mice, DC‐specific overexpression Irf8...

10.1002/advs.202416238 article EN cc-by Advanced Science 2025-04-04

Drug delivery across the blood-brain barrier is limited by several mechanisms. One important mechanism drug efflux, mediated transport proteins, including P-glycoprotein. The goal of this work was to examine effect a novel system, Pluronic block copolymer P85, on P-glycoprotein-mediated efflux from brain using in vitro and vivo methods. hypothesis that specific systems enhance central nervous system through inhibition P85 cellular accumulation digoxin, model P-glycoprotein substrate,...

10.1016/s0022-3565(24)38781-6 article EN Journal of Pharmacology and Experimental Therapeutics 2001-02-01

Viral infection leads to activation of the transcription factors interferon regulatory factor-3 and NF-kappaB, which collaborate induce type I IFNs. The RNA helicase proteins RIG-I MDA5 were recently identified as two cytoplasmic viral sensors that recognize different species RNAs produced during replication. In this study, we DAK, a functionally unknown dihydroacetone kinase, specific MDA5-interacting protein. DAK was associated with MDA5, but not RIG-I, under physiological conditions....

10.1073/pnas.0700544104 article EN Proceedings of the National Academy of Sciences 2007-06-29

Pluronic block copolymers are potent sensitizers of multidrug resistant cancers. SP1049C, a Pluronic-based micellar formulation doxorubicin (Dox) has completed Phase II clinical trial and demonstrated safety efficacy in patients with advanced adenocarcinoma the esophagus gastroesophageal junction. This study elucidates ability SP1049C to deplete cancer stem cells (CSC) decrease tumorigenicity vivo.P388 murine leukemia ascitic tumor was grown BDF1 mice. The animals were treated with: (a)...

10.1371/journal.pone.0072238 article EN cc-by PLoS ONE 2013-08-19

Foot-and-mouth disease is a frequently occurring of cloven-hoofed animals that caused by infection with the foot-and-mouth virus (FMDV). FMDV circumvents type-I IFN response expressing proteins antagonize cellular innate immunity, such as leader protease and 3C protease. We identified structural protein VP3 negative regulator virus-triggered IFN-β signaling pathway. Expression inhibited Sendai activation regulatory factor-3 expression retinoic acid-inducible gene-I/melanoma...

10.1096/fj.15-281410 article EN The FASEB Journal 2016-01-26

Hepatitis C virus (HCV) infection is a major cause of human chronic liver disease and hepatocellular carcinoma. G-quadruplex (G4) an important four-stranded secondary structure nucleic acids. Recently, we discovered that the core gene HCV contains G4 RNA structure; however, interaction between host cellular proteins, roles in pathogenesis remain elusive. Here, identified protein, nucleolin (NCL), which bound stabilized structure. We demonstrated direct colocalization NCL wild-type at both...

10.1093/nar/gky1177 article EN cc-by Nucleic Acids Research 2018-11-17

Abstract Foot-and-mouth disease virus (FMDV) is the etiological agent of FMD, which affects cloven-hoofed animals. The pathophysiology FMDV has not been fully understood and evasion host innate immune system still unclear. Here, non-structural protein 3A was identified as a negative regulator virus-triggered IFN-β signaling pathway. Overexpression inhibited Sendai activation IRF3 expressions RIG-I/MDA5. Transient transfection co-immunoprecipitation experiments suggested that interacts with...

10.1038/srep21888 article EN cc-by Scientific Reports 2016-02-17

Abstract Glycine decarboxylase (GLDC) is a key enzyme of glycine cleavage system that converts into one-carbon units. GLDC commonly up-regulated and plays important roles in many human cancers. Whether how regulated by post-translational modifications unknown. Here we report mechanistic target rapamycin complex 1 (mTORC1) signal inhibits acetylation at lysine (K) 514 inducing transcription the deacetylase sirtuin 3 (SIRT3). Upon inhibition mTORC1, acetyltransferase acetyl-CoA (ACAT1)...

10.1038/s41467-021-24321-3 article EN cc-by Nature Communications 2021-07-09

Viral infection causes activation of the transcription factors NF-κB and IRF3, which collaborate to induce type I interferons (IFNs) cellular antiviral response. The mitochondrial outer membrane protein VISA acts as a critical adapter for assembling virus-induced complex that signals IRF3 activation. Using biochemical purification approach, we identified WD repeat WDR5 VISA-associated protein. was recruited in viral dependent manner. also caused translocation from nucleus mitochondria....

10.1073/pnas.0908967107 article EN Proceedings of the National Academy of Sciences 2009-12-22

Transcription factor IRF3-mediated type I interferon induction is essential for antiviral innate immunity. We identified the deSUMOylating enzyme Sentrin/SUMO-specific protease (SENP) 2 as a negative regulator of virus-triggered IFN-β induction. Overexpression SENP2 caused IRF3 deSUMOylation, K48-linked ubiquitination, and degradation, whereas depletion had opposite effects. Both SUMOylation ubiquitination occurred at lysines 70 87, these processes are competitive. The level was markedly...

10.1093/jmcb/mjr020 article EN Journal of Molecular Cell Biology 2011-10-01
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