ArticleJournal of viral hepatitis2014
Identification of novel human kinases that suppress hepatitis C virus infection.
Article in Journal of viral hepatitis, 2014. 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
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
1 citing paper in PubMed, 5 citations in OpenAlex.
- The elusive function of the hepatitis C virus p7 protein.Virology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The human kinome includes between 500 and 600 known kinases and open reading frames (ORFs) that play key roles in regulating many cellular processes. Past studies adopting loss-of-function approaches have identified some kinases whose activities are required for hepatitis C virus (HCV) life cycle. Here, by screening a retroviral cDNA library of 192 active human kinases, we found that three of them, namely cyclin-dependent kinases regulatory subunit 1 (CKS1B), mitogen-activated protein kinase kinase 5 (MAP2K5) and protein kinase C and casein kinase substrate in neurons 1 (PACSIN1), potently suppressed HCV infection. The expression of these kinases did not induce the production of type I interferon (IFN) and interferon-stimulated genes (ISGs); instead, they inhibited HCV at postentry stages. Specifically, CKS1B and MAP2K5 significantly inhibited viral RNA replication. PACSIN1, by contrast, inhibited HCV infection by decreasing the level of HCV p7. Altogether, the identification of human protein kinases that exert an anti-HCV activity highlighted the potential of combating HCV infection by activating specific kinase-mediated pathways, offering an alternative strategy of treatment.
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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.