Membrane-associated RING-CH (MARCH) family member proteins are RING-finger E3 ubiquitin ligases that are known to downregulate cellular transmembrane proteins. MARCH8 is a novel antiviral factor that inhibits HIV-1 envelope glycoprotein and vesicular stomatitis virus G by downregulating these envelope glycoproteins from the cell surface, resulting in their reduced incorporation into virions. More recently, we have found that MARCH8 reduces viral infectivity via two different mechanisms. Additionally, several groups have reported further antiviral or virus-supportive functions of the MARCH8 protein and its other cellular mechanisms. In this review, we summarize the current knowledge about the molecular mechanisms by which MARCH8 can regulate cellular homeostasis and inhibit and occasionally support enveloped virus infection.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/febs.16017 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
MARCH8 Restricts RSV Replication by Promoting Cellular Apoptosis Through Ubiquitin-Mediated Proteolysis of Viral SH Protein.
Viruses
December 2024
Department of Virology 3, National Institute of Infectious Diseases, Musashimurayama 208-0011, Tokyo, Japan.
Numerous host factors function as intrinsic antiviral effectors to attenuate viral replication. MARCH8 is an E3 ubiquitin ligase that has been identified as a host restriction factor that inhibits the replication of various viruses. This study elucidated the mechanism by which MARCH8 restricts respiratory syncytial virus (RSV) replication through selective degradation of the viral small hydrophobic (SH) protein.
View Article and Find Full Text PDFUbiquitination and degradation of MHC-II by Tim-3 inhibits antiviral immunity.
Cell Immunol
January 2025
Beijing Institute of Basic Medical Sciences, Beijing, China. Electronic address:
We previously reported that Tim-3, an immune checkpoint inhibitor, inhibits MHC-II expression, but the molecular mechanisms involved and the implications for antiviral immunity remain to be determined. Here, we found that during H1N1 infection, Tim-3 inhibits MHC-II expression in macrophages/microglia in vitro. Tim-3 interacts with MHC-II via its intracellular tail and induces proteasomal dependent degradation of MHC-II.
View Article and Find Full Text PDFNPR1 promotes cisplatin resistance by inhibiting PARL-mediated mitophagy-dependent ferroptosis in gastric cancer.
Cell Biol Toxicol
October 2024
Department of Gastrointestinal Surgery, The First Affiliated Hospital, Yijishan Hospital of Wannan Medical College, No.2, Zheshan West Road, Wuhu, 241001, Anhui, China.
Cisplatin-based chemotherapy serves as the standard of care for individuals with advanced stages of gastric cancer. Nevertheless, the emergence of chemoresistance in GC has detrimental impacts on prognosis, yet the underlying mechanisms governing this phenomenon remain elusive. Level of mitophagy and ferroptosis of GC cells were detected by fluorescence, flow cytometry, GSH, MDA, Fe assays, and to explore the specific molecular mechanisms between NPR1 and cisplatin resistance by performing western blot and coimmunoprecipitation (co-IP) assays.
View Article and Find Full Text PDFNLRP12 inhibits PRRSV-2 replication by promoting GP2a degradation via MARCH8.
Vet Microbiol
November 2024
Key Laboratory of Veterinary Biological Products, College of Veterinary Medicine, Henan University of Animal Husbandry and Economy, Zhengzhou, China. Electronic address:
NLRP12, a member of the NLR family, has been shown to exert a vital function in orchestrating immune responses. Here, using the immunosuppressive porcine reproductive and respiratory syndrome virus (PRRSV) as a model, the role of NLRP12 in virus infection was deciphered. We demonstrated that overexpression of NLRP12 significantly restrained PRRSV replication, while NLRP12 silencing resulted in increased viral titer.
View Article and Find Full Text PDFMARCH8 Mediates K27-Linked Polyubiquitination of IL-7 Receptor α to Negatively Regulate IL-7-Triggered T Cell Homeostasis.
J Immunol
November 2024
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China; Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; and Research Unit of Innate Immune and Inflammatory Diseases (2019RU063), Chinese Academy of Medical Sciences, Wuhan, China.
IL-7 is a cytokine produced by stromal cells, which binds to IL-7Rα and plays an important role for homeostasis of T lymphocytes. Excessive activities of IL-7-triggered signaling pathways causes autoimmune diseases. How IL-7-triggered signaling and immune effects are regulated is not fully understood.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!