ArticleJournal of virology2025
Tankyrases positively regulate influenza A virus replication via type I interferon response.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- NADThe Journal of general virology · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Influenza viruses are respiratory pathogens that cause both seasonal and unpredictable pandemic infections in humans. Currently approved anti-influenza drugs target the viral proteins. A recurrent mutation in the influenza genome leads to drug resistance and thus hinders the efficacy of anti-influenza drug treatments. Influenza A virus (IAV) depends on host factors to complete its virus life cycle. Thus, there are increasing interests in antiviral drugs that target host cellular proteins required for virus replication. Poly (ADP-ribose) polymerases (PARPs) are the host factors that modify protein functions by adding ADP-ribose to target proteins. Using the CRISPR activation system, we screened all 17 PARP members for its effects on IAV infection in lung epithelial A549 cells. Tankyrase 1 and 2 (TNKS 1/2 or PARP5A/5B) were found to be potent proviral factors. Knockout of TNKS1 or TNKS2 in HEK293T cells by CRISPR reduced viral mRNA and protein levels in cells and viral titers in culture media. Double knockout of TNKS1 and TNKS2 had a larger effect on IAV infection than single knockout of each isoform. The effect of TNKS double knockout on IAV replication was strain independent. Overexpression of TNKS1/2 in the double knockout cells restored the IAV replication to a level similar to the control cells. TNKS double knockout activated JNK/c-Jun signaling, enhanced Stat signaling, and increased type I interferon expression. Finally,
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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 Socratic graph.