Ya-Ling Xing

China Institute for Radiation Protection, Peping, Beijing, China

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Publications (7)9.89 Total impact

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    ABSTRACT: The mitochondrial antiviral signaling adaptor, MAVS, also known as Cardif, VISA or IPS1, is critical for host defenses against viral infection by inducing expression of type-1 interferons (IFN-I). The sensors of antiviral immunity, RIG-I and melanoma differentiation-associated gene 5(MDA5), detect the invasion pathogens, and pass the signal to MAVS, which is anchored to the mitochondrial membrane. MAVS then stimulates TBK1 and IKK complex and activates the transcription factors of IRF3/7 and NF-kB, which lead to the expression of interferon and activate antiviral innate immunity. MAVS was recently found to localize in both peroxisome and mitochondrial membrane. The peroxisomal MAVS is required for the rapid induction of antiviral effectors, whereas the mitochondrial MAVS is required for a sustained antiviral immunity response. This review focused on the discovery, domain structure and cellular localization of MAVS with an emphasis on the regulatory mechanisms of MAVS in modulating the antiviral innate immunity.
    No preview · Article · May 2013 · ACTA AGRONOMICA SINICA
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    ABSTRACT: STING (stimulator of interferon genes) is a novel regulatory protein in innate immune signaling pathways, which has been shown to be essential for the production of type I interferon in response to certain viruses and intracellular bacteria. B type dsDNA and 5 ' -3p dsRNA are detected by the corresponding pattern recognition receptors (PRRs) after exposing to host cells, which pass signals to STING. STING then recruits TBK1 to activate IRF3 and induce IFN by the similar mechanism. Besides, STING can be a PRR of the cyclic dinucleotides, such as c-di-GMP and c-di-AMP in bacteria, to induce type I interferon response. Except IFN, STING also activates STAT6 to induce some specific chemokines capable of attracting various immune cells. Here, we review recent studies on STING's structure, location, function, and regulatory mechanisms in the innate immune pathway, which provide an important theoretical guidance for the development of new antiviral immunotherapy.
    No preview · Article · Jan 2013 · ACTA AGRONOMICA SINICA
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    ABSTRACT: Apoptosis of vascular endothelial cells results in the loss of endothelial integrity, and is a risk factor of atherosclerosis (AS). Lipopolysaccharide (LPS) stimulates inflammation during AS. The current study examined the effect of a potent water-soluble antioxidant, protocatechuic aldehyde (PCA; derived from the Chinese herb Salvia miltiorrhiza) on apoptosis in human umbilical vein endothelial cells (HUVECs) stimulated with LPS. The LPS (15 µg/ml) stimulation for 30 h resulted in significant HUVEC apoptosis, as detected by Hoechst 33258 staining and Annexin V analysis. The PCA (0.25-1.0 mmol/L, 12 h) inhibited LPS-induced HUVEC apoptosis in a dose-dependent manner. Lipopolysaccharide induced caspase-3 activation, but had no significant effect on caspase-2, Bcl-2/Bax, cytochrome c, caspase-9 and granzyme B expression. Protocatechuic aldehyde (0.25-1.0 mmol/L) significantly inhibited caspase-3 activation in a dose-dependent manner. A specific caspase-3 inhibitor also protected against LPS-induced apoptosis; however, no cooperative effect of PCA and the inhibitor was observed in this study. Collectively, these results indicate that PCA inhibits LPS-induced apoptosis in HUVECs through a mechanism that involves caspase-3. Copyright © 2012 John Wiley & Sons, Ltd.
    No preview · Article · Sep 2012 · Phytotherapy Research
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    ABSTRACT: So far there are at least five coronaviruses that are responsible for human respiratory infections. The pathogenesis and immunity of Coronavirus are the result of interaction between virus and host. The innate immune response will be started when coronaviruses infect cells. Coronaviruses usually encode multifunctional proteins that are critical for viral replication and blocking the innate immune response to viral infection. Human Coronavirus NL63 (HCoV-NL63), a new-emerging human Coronavirus for human respiratory infections, has two papain-like protease (PLP) core domains, PLP1 and PLP2, in nonstructural protein nsp3. Besides the proteolytic processing activity towards pp1a(lab), it was previously demonstrated that PLP2 of HCoV-NL63 has in vitro deubiquitinase (DUB) activity. However, the characteristics and functions of DUB activity of NL63 Coronavirus PLPs are poorly understood. It was first demonstrated that the core domain of PLP2, but not PLP1, has in vivo DUB activity, and the DUB activity is not dependent on the catalytic residue of D1849. However, the PLP2 DUB activity is significantly reduced when the catalytic sites of C1678 and H1836 were mutated. PLP2 has both in vivo DUB and DeISGylation activity, and PLP2 exhibits DUB activity toward ubiquitinated branched peptides without any specificity for either Lys48 linkages or Lys63 linkages. Furthermore, PLP2, but not PLP1, is the only core domain responsible for the inhibition of both RIG-I and TLR3-dependent induction of IFNα/β expression. Mechanism study demonstrated that PLP2 interacts with the key regulation players of RIG-I and ERIS (also called STING/MITA) of IFN induction pathway, and induces the deubiquitination of RIG-I and ERIS. Overall, these results definitely demonstrated that for the two core domains of PLP responsible for proteolytically processing of N-terminal part of ppla(lab) of NL63 Coronavirus, PLP2 is the only core domain of PLPs that responsible for DUB activity and IFN antagonists. The studies are currently underway to determine the biological significance of DUB of NL63 Coronavirus PLP2 in virus replication and pathogenesis.
    No preview · Article · Aug 2010 · Progress in Biochemistry and Biophysics
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    ABSTRACT: Emerging and re-emerging human viral pathogens, such as severe acute respiratory syndrome (SARS), which emerged in 2003, and the recently emerged swine-origin H1N1 influenza virus, which causes global pandemics, have had a worldwide impact and therefore represent a serious threat to human health. Viruses as the obligate parasites strictly depend on host cells for replication and, throughout co-evolution with hosts, viruses have developed strategies to evade and subvert the host antiviral innate immune response. A wide variety of RNA viruses have been reported to encode proteins that inhibit host innate immune responses. Papain-like protease (PLP) of human coronavirus is a novel viral-encoded deubiquitinase and is an IFN antagonist for inhibition of host antiviral innate immune response through disruption of ERIS (also called MITA/STING)-mediated signaling. The novel mechanisms by which human coronavirus inhibits host IFN response and new findings that papain-like protease (PLP) of coronavirus is an IFN antagonist which targets specific components of the IFN induction pathway were introduced.
    No preview · Article · Mar 2010 · Progress in Biochemistry and Biophysics
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    ABSTRACT: This article has been withdrawn at the request of the authors. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.
    Preview · Article · Aug 2008 · European journal of pharmacology
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    ABSTRACT: Oxidative stress caused by dopamine may play an important role in the pathogenesis of Parkinson's disease. Salvianolic acid B is an antioxidant derived from the Chinese herb, Salvia miltiorrhiza. In this study, we investigated the neuroprotective effect of salvianolic acid B against 6-hydroxydopamine-induced cell death in human neuroblastoma SH-SY5Y cells. Pretreatment of SH-SY5Y cells with salvianolic acid B significantly reduced 6-hydroxydopamine-induced generation of reactive oxygen species, and prevented 6-hydroxydopamine-induced increases in intracellular calcium. Our data demonstrated that 6-hydroxydopamine-induced apoptosis was reversed by salvianolic acid B treatment. Salvianolic acid B reduced the 6-hydroxydopamine-induced increase of caspase-3 activity, and reduced cytochrome C translocation into the cytosol from mitochondria. The 6-hydroxydopamine-induced decrease in the Bcl-x/Bax ratio was prevented by salvianolic acid B. Additionally, salvianolic acid B decreased the activation of extracellular signal-regulated kinase and induced the activation of 6-hydroxydopamine-suppressed protein kinase C. These results indicate that the protective function of salvianolic acid B is dependent upon its antioxidative potential. Our results strongly suggest that salvianolic acid B may be effective in treating neurodegenerative diseases associated with oxidative stress.
    No preview · Article · Feb 2008 · The International Journal of Biochemistry & Cell Biology