ArticleJournal of virology2010
Two overlapping domains of a lyssavirus matrix protein that acts on different cell death pathways.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 29 citations in OpenAlex.
- Oncolytic Effects of S89K Matrix Protein of Vesicular Stomatitis Virus in Cervical Cancer.Advanced biomedical research · 2026Article
- Review
- Lyssavirus M protein degrades neuronal microtubules by reprogramming mitochondrial metabolism.mBio · 2024Article
- Regulation of NF-κB by the p105-ABIN2-TPL2 complex and RelAp43 during rabies virus infection.PLoS pathogens · 2017Article
- The matrix protein of rabies virus binds to RelAp43 to modulate NF-κB-dependent gene expression related to innate immunity.Scientific reports · 2016Article
- Wild-type rabies virus induces autophagy in human and mouse neuroblastoma cell lines.Autophagy · 2016Article
- Subversion of the Immune Response by Rabies Virus.Viruses · 2016Review
- Systems Biomedicine of Rabies Delineates the Affected Signaling Pathways.Frontiers in microbiology · 2016Article
- Rabies virus phosphoprotein interacts with mitochondrial Complex I and induces mitochondrial dysfunction and oxidative stress.Journal of neurovirology · 2015Article
- RelAp43, a member of the NF-κB family involved in innate immune response against Lyssavirus infection.PLoS pathogens · 2012Article
- Purification and characterization of a recombinant bacteriophytochrome of Xanthomonas oryzae pathovar oryzae.The protein journal · 2011Article
- Rabies, still neglected after 125 years of vaccination.PLoS neglected tropical diseases · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lyssavirus matrix (M) protein induces apoptosis. The regions of the M protein that are essential for triggering cell death pathways are not yet clearly defined. We therefore compared the M proteins from two viruses that have contrasting characteristics in terms of cellular apoptosis: a genotype 3 lyssavirus, Mokola virus (MOK), and a genotype 1 rabies virus isolated from a dog from Thailand (THA). We identified a 20-amino-acid fragment (corresponding to positions 67 to 86) that retained the cell death activities of the full-length M protein from MOK via both the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and inhibition of cytochrome c oxidase (CcO) activity. We found that the amino acids at positions 77 and 81 have an essential role in triggering these two cell death pathways. Directed mutagenesis demonstrated that the amino acid at position 77 affects CcO activity, whereas the amino acid at position 81 affects TRAIL-dependent apoptosis. Mutations in the full-length M protein that compromised induction of either of these two pathways resulted in delayed apoptosis compared with the time to apoptosis for the nonmutated control.
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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.