ArticleInternational journal of molecular sciences2024
TRIM44 Promotes Rabies Virus Replication by Autophagy-Dependent Mechanism.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- TRIM7 Inhibits Rabies Virus Replication by Promoting K48-Linked Ubiquitination and Degradation of RABV-M.Emerging microbes & infections · 2026Article
- TRIM proteins: A 'swiss army knife' of antiviral immunity.PLoS pathogens · 2025Review
- Selective Autophagy Mediated by Protein Ubiquitination in Major Prevalent Zoonoses.Transboundary and emerging diseases · 2025Review
- scTRIM44 Positively Regulated Siniperca Chuatsi Rhabdovirus Through RIG-I- and MDA5-Mediated Interferon Signaling.Viruses · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
Tripartite motif (TRIM) proteins are a multifunctional E3 ubiquitin ligase family that participates in various cellular processes. Recent studies have shown that TRIM proteins play important roles in regulating host-virus interactions through specific pathways, but their involvement in response to rabies virus (RABV) infection remains poorly understood. Here, we identified that several TRIM proteins are upregulated in mouse neuroblastoma cells (NA) after infection with the rabies virus using RNA-seq sequencing. Among them, TRIM44 was found to regulate RABV replication. This is supported by the observations that downregulation of TRIM44 inhibits RABV replication, while overexpression of TRIM44 promotes RABV replication. Mechanistically, TRIM44-induced RABV replication is brought about by activating autophagy, as inhibition of autophagy with 3-MA attenuates TRIM44-induced RABV replication. Additionally, we found that inhibition of autophagy with rapamycin reverses the TRIM44-knockdown-induced decrease in LC3B expression and autophagosome formation as well as RABV replication. The results suggest that TRIM44 promotes RABV replication by an autophagy-dependent mechanism. Our work identifies TRIM44 as a key host factor for RABV replication, and targeting TRIM44 expression may represent an effective therapeutic strategy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.