BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
Veterinary Research, ISSN: 1297-9716, Vol: 47, Issue: 1, Page: 47
2016
- 24Citations
- 18Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations24
- Citation Indexes24
- 24
- CrossRef12
- Captures18
- Readers18
- 18
- Mentions1
- News Mentions1
- 1
Most Recent News
PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
Abstract Bovine herpesvirus 1 (BoHV-1) productive infection stimulates β-catenin-dependent transcription to facilitate virus replication. Phosphoglycerate kinase 1 (PGK1), which catalyses the initial step of ATP
Article Description
The levels of cellular reactive oxygen species (ROS) and ATP as well as the mitochondrial membrane potential (MMP) in response to bovine herpesvirus 1 (BHV-1) infection of MDBK cells were measured, respectively. BHV-1 infection increased ROS production which depended on viral entry, and de novo protein expression and/or DNA replication. Vice versa, excessive ROS was required for efficient viral replication. Levels of both ATP and MMP were significantly decreased after BHV-1 infection. Interestingly, the loss of MMP was ameliorated by ROS depression. Collectively, ROS dependent mitochondrial damage and ultimately disruption of energy metabolism (ATP depletion) are a potential pathogenic mechanism for BHV-1 infection.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84961616032&origin=inward; http://dx.doi.org/10.1186/s13567-016-0332-2; http://www.ncbi.nlm.nih.gov/pubmed/27000063; http://www.veterinaryresearch.org/content/47/1/47; https://dx.doi.org/10.1186/s13567-016-0332-2; https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-016-0332-2
Springer Science and Business Media LLC
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