ArticleJournal of virology2013
Cellular chaperonin CCTγ contributes to rabies virus replication during infection.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
- Participation of host cell proteins in inclusion bodies of non-segmented RNA virus infected cells: a molecular insight.Virology journal · 2025Review
- The recruitment of TRiC chaperonin in rotavirus viroplasms correlates with virus replication.mBio · 2024Article
- Quantitative analysis of acetylation in peste des petits ruminants virus-infected Vero cells.Virology journal · 2023Article
- Chaperonin TRiC/CCT Participates in Mammarenavirus Multiplication in Human Cells via Interaction with the Viral Nucleoprotein.Journal of virology · 2023Article
- Mechanistic insights into protein folding by the eukaryotic chaperonin complex CCT.Biochemical Society transactions · 2022Review
- Deconstructing virus condensation.PLoS pathogens · 2021Review
- Diversity in heat shock protein families: functional implications in virus infection with a comprehensive insight of their role in the HIV-1 life cycle.Cell stress & chaperones · 2021Review
- Article
- Rabies Infection: An Overview of Lyssavirus-Host Protein Interactions.Iranian biomedical journal · 2021Review
- Enterovirus-A71 exploits peripherin and Rac1 to invade the central nervous system.EMBO reports · 2021Article
- Human Papillomavirus infection requires the CCT Chaperonin Complex.Journal of virology · 2021Article
- Negri bodies and other virus membrane-less replication compartments.Biochimica et biophysica acta. Molecular cell research · 2020Review
- The Role of Molecular Chaperones in Virus Infection and Implications for Understanding and Treating COVID-19.Journal of clinical medicine · 2020Review
- Rabies virus phosphoprotein P5 binding to BECN1 regulates self-replication by BECN1-mediated autophagy signaling pathway.Cell communication and signaling : CCS · 2020Article
- TRiC/CCT Complex, a Binding Partner of NS1 Protein, Supports the Replication of Zika Virus in Both Mammalians and Mosquitoes.Viruses · 2020Article
- Proteostasis in Viral Infection: Unfolding the Complex Virus-Chaperone Interplay.Cold Spring Harbor perspectives in biology · 2020Review
- Hsp70 Is a Potential Therapeutic Target for Echovirus 9 Infection.Frontiers in molecular biosciences · 2020Article
- Article
- Knockdown ofFrontiers in microbiology · 2019Article
- Chaperoning theViruses · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rabies, as the oldest known infectious disease, remains a serious threat to public health worldwide. The eukaryotic cytosolic chaperonin TRiC/CCT complex facilitates the folding of proteins through ATP hydrolysis. Here, we investigated the expression, cellular localization, and function of neuronal CCTγ during neurotropic rabies virus (RABV) infection using mouse N2a cells as a model. Following RABV infection, 24 altered proteins were identified by using two-dimensional electrophoresis and mass spectrometry, including 20 upregulated proteins and 4 downregulated proteins. In mouse N2a cells infected with RABV or cotransfected with RABV genes encoding nucleoprotein (N) and phosphoprotein (P), confocal microscopy demonstrated that upregulated cellular CCTγ was colocalized with viral proteins N and P, which formed a hollow cricoid inclusion within the region around the nucleus. These inclusions, which correspond to Negri bodies (NBs), did not form in mouse N2a cells only expressing the viral protein N or P. Knockdown of CCTγ by lentivirus-mediated RNA interference led to significant inhibition of RABV replication. These results demonstrate that the complex consisting of viral proteins N and P recruits CCTγ to NBs and identify the chaperonin CCTγ as a host factor that facilitates intracellular RABV replication. This work illustrates how viruses can utilize cellular chaperonins and compartmentalization for their own benefit.
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Registered trials
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.