Molecular characterization and functional analysis of duck CCCH-type zinc finger antiviral protein (ZAP)

2021 ◽  
Vol 561 ◽  
pp. 52-58
Author(s):  
Rongrong Zhang ◽  
Yan He ◽  
Xinyu Zhu ◽  
Guoyuan Wen ◽  
Qingping Luo ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Molecular Characterization ◽  
Zinc Finger ◽  
Antiviral Protein

Cloning and functional analysis of SCTF-1 encoding a C2H2-type zinc finger protein from soybean

2012 ◽  
Vol 34 (6) ◽  
pp. 749-756 ◽  
Author(s):  
Bing SONG ◽  
Pi-Wu WANG ◽  
Yong-Ping FU ◽  
Xu-Hong FAN ◽  
Hai-Feng XIA ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

Cloning, Molecular Characterization, Functional Analysis of Wheat TaVIP1 Genes

2017 ◽  
Vol 43 (2) ◽  
pp. 201
Author(s):  
Pei ZHAO ◽  
Li-Jie TENG ◽  
Ke WANG ◽  
Li-Pu DU ◽  
Xian REN ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Molecular Characterization

scholarly journals Molecular characterization and functional analysis of fourβ-1,4-endoglucanases from the root-lesion nematodePratylenchus vulnus

2014 ◽  
Vol 63 (6) ◽  
pp. 1436-1445 ◽  
Author(s):  
E. Fanelli ◽  
A. Troccoli ◽  
E. Picardi ◽  
C. Pousis ◽  
F. De Luca
Keyword(s):  
Functional Analysis ◽  
Molecular Characterization

Molecular characterization and functional analysis of Eimeria tenella citrate synthase

2021 ◽  
Vol 120 (3) ◽  
pp. 1025-1035
Author(s):  
Haixia Wang ◽  
Qiping Zhao ◽  
Shunhai Zhu ◽  
Hui Dong ◽  
Shuilan Yu ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Molecular Characterization ◽  
Citrate Synthase ◽  
Eimeria Tenella

scholarly journals Inhibition of Japanese encephalitis virus infection by the host zinc-finger antiviral protein

2018 ◽  
Vol 14 (7) ◽  
pp. e1007166 ◽  
Author(s):  
Hsin-Ping Chiu ◽  
Han Chiu ◽  
Chao-Fu Yang ◽  
Yi-Ling Lee ◽  
Feng-Lan Chiu ◽  
...  
Keyword(s):  
Virus Infection ◽  
Japanese Encephalitis Virus ◽  
Zinc Finger ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Antiviral Protein ◽  
Japanese Encephalitis Virus Infection

Expression of Zinc-Finger Antiviral Protein in hCMEC/D3 Human Cerebral Microvascular Endothelial Cells: Effect of a Toll-Like Receptor 3 Agonist

2021 ◽  
pp. 1-10
Author(s):  
Mako Okudera ◽  
Minami Odawara ◽  
Masashi Arakawa ◽  
Shogo Kawaguchi ◽  
Kazuhiko Seya ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Zinc Finger ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Toll Like Receptor ◽  
Antiviral Protein ◽  
Polycytidylic Acid ◽  
Microvascular Endothelial ◽  
The Brain

<b><i>Introduction:</i></b> Invasion of viruses into the brain causes viral encephalitis, which can be fatal and causes permanent brain damage. The blood-brain barrier (BBB) protects the brain by excluding harmful substances and microbes. Brain microvascular endothelial cells are important components of the BBB; however, the mechanisms of antiviral reactions in these cells have not been fully elucidated. Zinc-finger antiviral protein (ZAP) is a molecule that restricts the infection of various viruses, and there are 2 major isoforms: ZAPL and ZAPS. Toll-like receptor 3 (TLR3), a pattern-recognition receptor against viral double-stranded RNA, is implicated in antiviral innate immune reactions. The aim of this study was to investigate the expression of ZAP in cultured hCMEC/D3 human brain microvascular endothelial cells treated with an authentic TLR3 agonist polyinosinic-polycytidylic acid (poly IC). <b><i>Methods:</i></b> hCMEC/D3 cells were cultured and treated with poly IC. Expression of ZAPL and ZAPS mRNA was investigated using quantitative reverse transcription-polymerase chain reaction, and protein expression of these molecules was examined using western blotting. The role of nuclear factor-κB (NF-κB) was examined using the NF-κB inhibitor, SN50. The roles of interferon (IFN)-β, IFN regulatory factor 3 (IRF3), tripartite motif protein 25 (TRIM25), and retinoic acid-inducible gene-I (RIG-I) in poly IC-induced ZAPS expression were examined using RNA interference. Propagation of Japanese encephalitis virus (JEV) was examined using a focus-forming assay. <b><i>Results:</i></b> ZAPS mRNA and protein expression was upregulated by poly IC, whereas the change of ZAPL mRNA and protein levels was minimal. Knockdown of IRF3 or TRIM25 decreased the poly IC-induced upregulation of ZAPS, whereas knockdown of IFN-β or RIG-I did not affect ZAPS upregulation. SN50 did not affect ZAPS expression. Knockdown of ZAP enhanced JEV propagation. <b><i>Conclusion:</i></b> ZAPL and ZAPS were expressed in hCMEC/D3 cells, and ZAPS expression was upregulated by poly IC. IRF3 and TRIM25 are involved in poly IC-induced upregulation of ZAPS. ZAP may contribute to antiviral reactions in brain microvascular endothelial cells and protect the brain from invading viruses such as JEV.

scholarly journals Cellular Zinc Finger Protein 622 Hinders Human Adenovirus Lytic Growth and Limits Binding of the Viral pVII Protein to Virus DNA

2018 ◽  
Vol 93 (3) ◽  
Author(s):  
Kwangchol Mun ◽  
Tanel Punga
Keyword(s):  
Life Cycle ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Human Adenovirus ◽  
Antiviral Protein ◽  
Viral Dna ◽  
Finger Protein ◽  
Wide Range ◽  
Infected Cells ◽  
Cellular Zinc

ABSTRACTHuman adenovirus (HAdV) encodes a multifunctional DNA-binding protein pVII, which is involved in virus DNA packaging and extracellular immune signaling regulation. Although the pVII is an essential viral protein, its exact role in the virus life cycle and interplay with cellular proteins have remained to a large extent unclear. We have recently identified the cellular zinc finger protein 622 (ZNF622) as a potential pVII-interacting protein. In this study, we describe the functional consequences of the ZNF622-pVII interplay and the role of ZNF622 in the HAdV life cycle. ZNF622 protein expression increased, and it accumulated similarly to the pVII protein in the nuclei of virus-infected cells. The lack of the ZNF622 protein specifically increased pVII binding to viral DNA in the infected cells and elevated the pVII protein levels in the purified virions. In addition, ZNF622 knockout cells showed an increased cell lysis and enhanced accumulation of the infectious virus particles. Protein interaction studies revealed that ZNF622 forms a trimeric complex with the pVII protein and the cellular histone chaperon protein nucleophosmin 1 (NPM1). The integrity of this complex is important since ZNF622 mutations and NPM1 deficiency changed pVII ability to bind viral DNA. Collectively, our results implicate that ZNF622 may act as a cellular antiviral protein hindering lytic HAdV growth and limiting pVII protein binding to viral DNA.IMPORTANCEHuman adenoviruses (HAdVs) are common human pathogens causing a wide range of acute infections. To counteract viral pathogenicity, cells encode a variety of antiviral proteins and noncoding RNAs to block virus growth. In this study, we show that the cellular zinc finger protein 622 (ZNF622) interacts with an essential HAdV protein known as pVII. This mutual interaction limits pVII binding to viral DNA. Further, ZNF622 has a role in HAdV life cycle since the lack of ZNF622 correlates with increased lysis of the infected cells and accumulation of the infectious virions. Together, our study reveals a novel cellular antiviral protein ZNF622, which may impede lytic HAdV growth.

scholarly journals Multiple Interferon Stimulated Genes Synergize with the Zinc Finger Antiviral Protein to Mediate Anti-Alphavirus Activity

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37398 ◽  
Author(s):  
Sophiya Karki ◽  
Melody M. H. Li ◽  
John W. Schoggins ◽  
Suyan Tian ◽  
Charles M. Rice ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Antiviral Protein ◽  
Interferon Stimulated Genes

Zinc finger antiviral protein inhibits coxsackievirus B3 virus replication and protects against viral myocarditis

2015 ◽  
Vol 123 ◽  
pp. 50-61 ◽  
Author(s):  
Min Li ◽  
Kepeng Yan ◽  
Lin Wei ◽  
Jie Yang ◽  
Chenyu Lu ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Virus Replication ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Antiviral Protein
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