C 2 H 2 -type zinc-finger protein BCL11B suppresses avian Leukosis virus subgroup J replication by regulating apoptosis.

Autor: Qiu L; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: 007621@yzu.edu.cn., Yang T; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: yt1144736744@163.com., Guo Q; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: DX120190114@yzu.edu.cn., Hua T; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: huatian0202@163.com., Bi Y; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: ylbi@yzu.edu.cn., Chu P; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: chupf@yzu.edu.cn., Bai H; College of Animal Science and Technology, Yangzhou University, Yangzhou, China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Institutes of Agricultural Science and Technology Development, Yangzhou University, Yangzhou 225009, China. Electronic address: bhowen1027@yzu.edu.cn., Chen S; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: mrrchen@yzu.edu.cn., Chang G; College of Animal Science and Technology, Yangzhou University, Yangzhou, China. Electronic address: gbchang1975@yzu.edu.cn.
Jazyk: angličtina
Zdroj: International journal of biological macromolecules [Int J Biol Macromol] 2024 Aug; Vol. 275 (Pt 1), pp. 133644. Date of Electronic Publication: 2024 Jul 02.
DOI: 10.1016/j.ijbiomac.2024.133644
Abstrakt: Apoptosis plays a crucial role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J), an avian oncogenic retrovirus, has been shown to suppress apoptosis while promoting its own replication. ALV-J induces myeloid tumors and hemangiomas in chickens resulting in significant economic losses for commercial layer and meat-type chicken production. B-cell lymphoma/leukemia 11B (Bcl11b) encodes a C 2 H 2 -type zinc finger protein-BCL11B, that exerts critical functions in cell proliferation, differentiation, and plays an essential role in the immune system. Previous study has been shown that Bcl11b is associated with ALV-J infection. In this study, we further investigated the pathological changes in ALV-J infected cells and examined the role and expression regulation of chicken Bcl11b. Our results demonstrate that Bcl11b, as an interferon-stimulated gene (ISG), encodes C 2 H 2 -type zinc finger protein BCL11B that promotes apoptosis to inhibit ALV-J infection. Additionally, gga-miR-1612 and gga-miR-6701-3p regulate apoptosis and are involved in ALV-J infection by targeting Bcl11b, thus revealing immune response strategies between the host and ALV-J. Although the underlying mechanisms require further validation, Bcl11b and its regulatory miRNAs are the first to demonstrate inhibition of ALV-J replication via apoptosis. BCL11B can a valuable target for treating diseases triggered by ALV-J infection.
Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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