Jiani Wei
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jiani Wei has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Qianxun Liu
School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330031, China
1 shared publication - Shantong Peng
School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330031, China
1 shared publication - Zhenzhen Xie
School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330031, China
1 shared publication
Latest Publications
- Open Access
The Function of TRIM25 in Antiviral Defense and Viral Immune Evasion
Tripartite motif (TRIM) 25 is a member of the TRIM E3 ubiquitin ligase family, which plays multiple roles in anti-tumor and antiviral defenses through various pathways. Its RBCC and SPRY/PRY domains work cooperatively for its oligomerization and subsequent activation of ligase activity. TRIM25 expression is regulated by several proteins and RNAs, and it functionally participates in the post-transcriptional and translational modification of antiviral regulators, such as RIG-I, ZAP, and avSGs. Conversely, the antiviral functions of TRIM25 are inhibited by viral proteins and RNAs through their interactions, as well as by the viral infection-mediated upregulation of certain miRNAs. Here, we review the antiviral functions of TRIM25 and highlight its significance regarding innate immunity, particularly in antiviral defense and viral immune evasion.
Open AccessThe Function of TRIM25 in Antiviral Defense and Viral Immune Evasion
Tripartite motif (TRIM) 25 is a member of the TRIM E3 ubiquitin ligase family, which plays multiple roles in anti-tumor and antiviral defenses through various pathways. Its RBCC and SPRY/PRY domains work cooperatively for its oligomerization and subsequent activation of ligase activity. TRIM25 expression is regulated by several proteins and RNAs, and it functionally participates in the post-transcriptional and translational modification of antiviral regulators, such as RIG-I, ZAP, and avSGs. Conversely, the antiviral functions of TRIM25 are inhibited by viral proteins and RNAs through their interactions, as well as by the viral infection-mediated upregulation of certain miRNAs. Here, we review the antiviral functions of TRIM25 and highlight its significance regarding innate immunity, particularly in antiviral defense and viral immune evasion.