ArticleCell communication and signaling : CCS2020
Rabies virus phosphoprotein P5 binding to BECN1 regulates self-replication by BECN1-mediated autophagy signaling pathway.
Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
- Selective Autophagy Mediated by Protein Ubiquitination in Major Prevalent Zoonoses.Transboundary and emerging diseases · 2025Review
- Review
- The roles and mechanisms of endoplasmic reticulum stress-mediated autophagy in animal viral infections.Veterinary research · 2024Review
- TRIM44 Promotes Rabies Virus Replication by Autophagy-Dependent Mechanism.International journal of molecular sciences · 2024Article
- Review
- Bif-1c Attenuates Viral Proliferation by Regulating Autophagic Flux Blockade Induced by the Rabies Virus CVS-11 Strain in N2a Cells.Microbiology spectrum · 2023Article
- An inactivated recombinant rabies virus chimerically expressed RBD induces humoral and cellular immunity against SARS-CoV-2 and RABV.Virologica Sinica · 2023Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- The Multi-Faceted Role of Autophagy During Animal Virus Infection.Frontiers in cellular and infection microbiology · 2022Review
- Rabies Infection: An Overview of Lyssavirus-Host Protein Interactions.Iranian biomedical journal · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRabies virus (RABV) is reported to encode five phosphoproteins (P), which are involved in viral genomic replication, axonal transport, oxidative stress, interferon antagonism, and autophagy induction. However, the functions of the different P proteins are poorly understood.
methodsImmunofluorescence staining and western blot were performed to detect the autophagy activity, the form of ring-like structure, and the colocalization of BECN1 and P. Co-immunoprecipitation was performed to detect the interaction between P and BECN1. QRT-PCR and TCID
resultsWe found that P5 attaches to N-terminal residues 1-139 of BECN1 (beclin1) on the BECN1 ring-like structure through amino acid residues 173-222 of P5. Subsequently, we found that P5-induced autophagosomes did not fuse with lysosomes. Becn1 silencing did not recover P5 overexpression-induced promotion of RABV replication. Mechanistically, RABV protein PΔN82 (P5) induced incomplete autophagy via the BECN1-mediated signaling pathway.
conclusionsOur data indicate that P5 binding to the BECN1 ring benefits RABV replication by inducing BECN1 signaling pathway-dependent incomplete autophagy, which provides a potential target for antiviral drugs against RABV. Video abstract.
Indexed as
Identifiers
What OpenQuestion holds
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.