ArticleProceedings of the National Academy of Sciences of the United States of America1998
A mutant cell line defective in response to double-stranded RNA and in regulating basal expression of interferon-stimulated genes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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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
16 citing papers in PubMed, 36 citations in OpenAlex.
- Caspase-8-mediated cleavage inhibits IRF-3 protein by facilitating its proteasome-mediated degradation.The Journal of biological chemistry · 2011Article
- Vesicular stomatitis virus has extensive oncolytic activity against human sarcomas: rare resistance is overcome by blocking interferon pathways.Journal of virology · 2011Article
- Differential utilization of NF-kappaB RELA and RELB in response to extracellular versus intracellular polyIC stimulation in HT1080 cells.BMC immunology · 2011Article
- Activation of the interferon response by human cytomegalovirus occurs via cytoplasmic double-stranded DNA but not glycoprotein B.Journal of virology · 2010Article
- Interferon-inducible protein, P56, inhibits HPV DNA replication by binding to the viral protein E1.The EMBO journal · 2008Article
- Hyaluronan-mediated leukocyte adhesion and dextran sulfate sodium-induced colitis are attenuated in the absence of signal transducer and activator of transcription 1.The American journal of pathology · 2008Article
- IRF-3 activation by Sendai virus infection is required for cellular apoptosis and avoidance of persistence.Journal of virology · 2008Article
- ICP0 prevents RNase L-independent rRNA cleavage in herpes simplex virus type 1-infected cells.Journal of virology · 2006Article
- Down-regulation of p53 by double-stranded RNA modulates the antiviral response.Journal of virology · 2005Article
- Complete, gene-specific siRNA libraries: production and expression in mammalian cells.RNA (New York, N.Y.) · 2005Article
- Analysis of genes induced by Sendai virus infection of mutant cell lines reveals essential roles of interferon regulatory factor 3, NF-kappaB, and interferon but not toll-like receptor 3.Journal of virology · 2005Article
- Bunyamwera virus nonstructural protein NSs counteracts interferon regulatory factor 3-mediated induction of early cell death.Journal of virology · 2003Article
- IRF-3-dependent, NFkappa B- and JNK-independent activation of the 561 and IFN-beta genes in response to double-stranded RNA.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Role for p53 in gene induction by double-stranded RNA.Journal of virology · 2001Article
- NF-kappaB activation by double-stranded-RNA-activated protein kinase (PKR) is mediated through NF-kappaB-inducing kinase and IkappaB kinase.Molecular and cellular biology · 2000Article
- Induction of apoptosis by double-stranded-RNA-dependent protein kinase (PKR) involves the alpha subunit of eukaryotic translation initiation factor 2 and NF-kappaB.Molecular and cellular biology · 1999Article
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
Abstract
Although much progress has been made in identifying the signaling pathways that mediate the initial responses to interferons (IFNs), much less is known about how IFN-stimulated genes (ISGs) are kept quiescent in untreated cells, how the response is sustained after the initial induction, and how ISG expression is down-regulated, even in the continued presence of IFN. We have used the cell sorter to isolate mutant cells with constitutively high ISG expression. A recessive mutant, P2.1, has higher constitutive ISG levels than the parental U4C cells, which do not respond to any IFN. Unexpectedly, P2.1 cells also are deficient in the expression of ISGs in response to double-stranded RNA (dsRNA). Electrophoretic mobility-shift assays revealed that the defect is upstream of the activation of the transcription factors NFkappaB and IFN regulatory factor 1. Analysis of the pivotal dsRNA-dependent serine/threonine kinase PKR revealed that the wild-type kinase is present and is activated normally in response to dsRNA in P2.1 cells. Together, these data suggest that the defect in P2.1 cells is either downstream of PKR or in a component of a distinct pathway that is involved both in activating multiple transcription factors in response to dsRNA and in regulating the basal expression of ISGs.
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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.