DOI . ORG {
}
Detected CMS Systems:
- Wordpress (1 occurrences)
- Hubspot (1 occurrences)
We began analyzing https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006145, but it redirected us to https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006145. The analysis below is for the second page.
Title[redir]:
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Description:
Author Summary Organisms have evolved various innate strategies to defend against pathogens. During virus infection, the cell senses the viral nucleic acid and produces type I interferon, which alerts the neighboring cells. Signaling of type I interferon triggers expression of a wide array of genes, some of which encode proteins that inhibit the replication of diverse virus families. It is not clear what determines the broad yet specific activity of these interferon-induced gene products. Identification of cellular cofactors and pathways required for the function of these broadly antiviral proteins would help elucidate their mechanisms. Here, we perform a genome wide knockdown screen to identify host factors important for the antiviral action of zinc finger antiviral protein (ZAP), a broad-spectrum inhibitory protein induced by interferon. We find that ZAP synergizes with host proteins with divergent functions and identify TRIM25 as a bona fide ZAP cofactor. TRIM25 binds to both splice isoforms of ZAP, and stimulates their ubiquitination and function by facilitating the ability of ZAP to block viral translation. Our data sheds light on the antiviral mechanism of ZAP and advances our understanding of host factor contributions to innate immune responses against viral infections.
Title[redir]:
No title found...
Description:
Author Summary Organisms have evolved various innate strategies to defend against pathogens. During virus infection, the cell senses the viral nucleic acid and produces type I interferon, which alerts the neighboring cells. Signaling of type I interferon triggers expression of a wide array of genes, some of which encode proteins that inhibit the replication of diverse virus families. It is not clear what determines the broad yet specific activity of these interferon-induced gene products. Identification of cellular cofactors and pathways required for the function of these broadly antiviral proteins would help elucidate their mechanisms. Here, we perform a genome wide knockdown screen to identify host factors important for the antiviral action of zinc finger antiviral protein (ZAP), a broad-spectrum inhibitory protein induced by interferon. We find that ZAP synergizes with host proteins with divergent functions and identify TRIM25 as a bona fide ZAP cofactor. TRIM25 binds to both splice isoforms of ZAP, and stimulates their ubiquitination and function by facilitating the ability of ZAP to block viral translation. Our data sheds light on the antiviral mechanism of ZAP and advances our understanding of host factor contributions to innate immune responses against viral infections.
Matching Content Categories {📚}
- Science
- Video & Online Content
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What CMS is doi.org built with?
Doi.org employs WORDPRESS.
But there are also traces of other content systems on the page (hubspot).
Traffic Estimate {📈}
What is the average monthly size of doi.org audience?
🏙️ Massive Traffic: 50M - 100M visitors per month
Based on our best estimate, this website will receive around 91,705,781 visitors per month in the current month.
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We see no obvious way the site makes money.
Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.
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Keywords {🔍}
trim, zap, cells, zaps, antiviral, fig, article, view, google, scholar, sinv, zapl, activity, pmid, pubmedncbi, protein, data, screen, proteins, viral, replication, sirna, ubiquitination, zchavknockout, expression, virus, genes, shown, host, cell, plos, rna, sirnas, type, domain, clones, totoluc, transfected, infected, epub, effects, trexhzap, luciferase, function, ubiquitin, mutants, isoforms, control, antibody, gene,
Topics {✒️}
biology health global approach plos pathog 13 plos pathog plos genet cookies plos medicine rig-i-mediated antiviral activity rnai high-throughput screens plos large-scale rnai screens zinc-finger antiviral protein t-rex-hzap cells transfected t-rex-hzap cell line genome-wide screens [21 open access article t-rex-rzapc88r cell lines protein n-terminal acetylation rig-i-dependent production parental zc3hav1-knockout 293t zc3hav1-knockout 293t cells zc3hav1-null 293t cells disrupt protein-protein interactions tetracycline-inducible protein expression requires trim25-mediated ubiquitination sds–polyacrylamide gel electrophoresis t-rex-hzap cells 7500 t-rex-hzap cells abrogate zap-mediated hbv vsv-g-expressing plasmids mirna-mediated translational silencing cas9-expressing px459 vector c-terminal v5 tag prk5-ha-ubiquitin-wt supporting information files post-translational protein modification cmr dpf mrm dpf cmr mrm zap-mediated mrna decay mediate anti-alphavirus activity increased viral replication intensity-based absolute quantitation zc3hav1-targeting sirna smartpools ha-tagged wild type prk5-ha-ubiquitin-k63 virus induces interferon-lambda trim25 domain-expressing constructs trim25lo zc3hav1-knockout clones e3 ligase-defective trim25
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