Acta Veterinaria et Zootechnica Sinica ›› 2023, Vol. 54 ›› Issue (7): 3118-3126.doi: 10.11843/j.issn.0366-6964.2023.07.042

• RESEARCH NOTES • Previous Articles    

Ubiquitinase of NF-κB Signal Pathway Regulated by Neuromedin B and Its Receptor NMBR during Influenza A Virus H9N2 Subtype Infection

TIAN Shimao, WAN Qianhui, XU Xiaodong, KONG Yingying, TIAN Ke, TANG Yubing, CHEN Jilong, YANG Guihong*   

  1. Key Laboratory of Fujian-Taiwan Animal Pathogen Biology, College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China
  • Received:2022-11-30 Online:2023-07-23 Published:2023-07-21

Abstract: Neuromedin B(NMB) and its receptor(NMBR) could inhibit the infection of influenza A virus(IAV) H1N1 subtype through activating the pathway of NF-κB signaling. However, the regulation of NMB and NMBR on the expression of ubiquitination ligases related with NF-κB signaling pathway remains unclear. To explore the effects of NMB and NMBR on regulating the ubiquitination ligases involved in NF-κB signaling pathway during IAV/H9N2 infection, the expression levels of E3 ubiquitin ligase mind bomb-2(MIB2) and ring finger protein 8(RNF8), deubiquitin enzyme cylindromatosis(CYLD) involved in NF-κB signaling pathway were analyzed using the methods of RT-PCR, qRT-PCR, and Western blot(WB), based on the sh-NMBR cells and NMB stimulating A549 cells during IAV/H9N2 infection. The results showed that the increased expression levels of RNF8 and CYLD, and the decreased levels of MIB2 and P65 phosphorylation were observed in sh-NMBR cells during H9N2 infection, while the decreased levels of RNF8 and CYLD, and the increased levels of MIB2 and P65 phosphorylation were confirmed in NMB stimulating A549 cells. These results indicated that NMB and NMBR could affect the function of NF-κB signaling pathway by regulating the expression levels of ubiquitination ligases and P65 phosphorylation during IAV/H9N2 infection, which could provide a theoretical basis for further studying the mechanism of NMB and NMBR on inhibiting influenza A virus.

Key words: neuromedin B, neuromedin B receptor, influenza A virus H9N2 subtype, E3 ubiquitination enzymes, P65 phosphorylation

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