Degradation of TRIM32 is Induced by RTA for Kaposi's Sarcoma-associated Herpesvirus Lytic Replication

Overview

Journal J Virol

Publisher American Society for Microbiology

Date 2024 May 8

PMID 38717113

Authors

Yulin Zhang

Zhongwei Dong

Feng Gu

Yifei Xu

Ying Li

Wen Sun

Wutian Rao

Shujuan Du

Caixia Zhu

Yuyan Wang

Fang Wei

Qiliang Cai

Affiliations

Soon will be listed here.

Abstract

Importance: TRIM32 is associated with many cancers and viral infections; however, the role of TRIM32 in viral oncogenesis remains largely unknown. In this study, we found that the expression of TRIM32 is elevated by Kaposi's sarcoma-associated herpesvirus (KSHV) in latency, and RTA (the master regulator of lytic replication) induces TRIM32 for proteasome degradation upon viral lytic reactivation. This finding provides a potential therapeutic target for KSHV-associated cancers.

Citing Articles

Unraveling the Kaposi Sarcoma-Associated Herpesvirus (KSHV) Lifecycle: An Overview of Latency, Lytic Replication, and KSHV-Associated Diseases.

Losay V, Damania B Viruses. 2025; 17(2).

PMID: 40006930 PMC: 11860327. DOI: 10.3390/v17020177.

TRIM Proteins: Key Regulators of Immunity to Herpesvirus Infection.

Sayyad Z, Acharya D, Gack M Viruses. 2024; 16(11).

PMID: 39599852 PMC: 11599090. DOI: 10.3390/v16111738.

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