Expressed Gene Clusters Associated with Cellular Sensitivity and Resistance Towards Anti-viral and Anti-proliferative Actions of Interferon

Khabar, Khalid S.A.; Al‐Haj, Latifa; Al-Zoghaibi, Fahad; Marie, Mohammad; Dhalla, Mohammad; Polyak, Stephen J.; Williams, Bryan R.G.

doi:10.1016/j.jmb.2004.07.065

Cited by 36 publications

(46 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interaction of type I IFN with the IFNAR results in activation of the receptor-associated kinases Tyk-2 and Jak-1, which phosphorylate the transcription factors Stat-1 and Stat-2 ( Figure 1). Stat-1 and Stat-2 associate with IRF-9 and form a complex (ISGF3) that interacts with IFNstimulated response elements in the promoters of hundreds of IFN-stimulated genes (24)(25)(26). Several other pathways are, however, also involved in the action of the IFNAR (24).…”

Section: Introductionmentioning

confidence: 99%

The type I interferon system in systemic lupus erythematosus

Rönnblom

Eloranta

Alm

2006

Arthritis & Rheumatism

304

246

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

The type I interferon system in systemic lupus erythematosus

Rönnblom

Eloranta

Alm

2006

Arthritis & Rheumatism

304

246

View full text Add to dashboard Cite

“…Recent studies have also suggested that long (27-29 bp) dsRNAs and shRNAs that enter the RNA interference (RNAi) pathway in a Dicerdependent fashion provide more efficient gene silencing than shorter, Dicer-independent substrates (Kim et al 2004;Siolas et al 2004). These studies (which demonstrated potent and specific gene silencing by longer duplexes and hairpins) were performed in tumor cell lines that are often characterized by a host of genetic abnormalities including defects in the IFN response pathway (Stojdl et al 2000;Khabar et al 2004;Zughaier et al 2005). In this work we have systematically examined the effects of dsRNA length on gene silencing, cell viability, and induction of the innate immune response in a range of cell lines.…”

Section: Introductionmentioning

confidence: 99%

Induction of the interferon response by siRNA is cell type– and duplex length–dependent

Reynolds¹,

Anderson²,

Vermeulen³

et al. 2006

RNA

298

201

View full text Add to dashboard Cite

Long (27-29-bp dsRNA) Dicer-dependent substrates have been identified as potent mediators of RNAi-induced gene knockdown in HEK293 and HeLa cells. As the lengths of these molecules are reported to be below the threshold generally regarded as necessary for induction of the mammalian interferon (IFN) response, these long siRNA are being considered as RNAi substrates in both research and therapeutic settings. In this report, we demonstrate that >23-bp dsRNA can influence cell viability and induce a potent IFN response (highlighted by a strong up-regulation of the dsRNA receptor, Toll-like receptor 3) in a cell typespecific manner. This finding suggests that the length threshold for siRNA induction of the IFN response is not fixed but instead varies significantly among different cell types. Given the diversity of cell types that comprise whole organisms, these findings suggest great care should be taken when considering length variations of dsRNA molecules for RNAi experimentation, especially in therapeutic applications.

show abstract

“…B Sequences of putative ARE regions in the 3′UTRs of type-I IFN including several sub-types of IFN-α. Underlined are AU-rich patterns such as pentamers or hexamers while sequences in Bold are ARE that matches possibly functional 13 nucleotide consensus [18,46,87]. IFN initiates a cascade of events that leads to transcription of many genes (IFN-stimulated genes, ISG) and also pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to suppression of viral mRNA and viral protein synthesis, IFNs possess a multiarray of functions that are reflected in the large number of IFN-stimulated genes [45,46]. IFN possesses both stimulatory and inhibitory functions on the immune system which include posttranscriptional regulation of gene expression, including mRNA stability and translation.…”

Section: Role Of Ifn In Post-transcriptional Control Of Cellular Genementioning

confidence: 99%

Post-transcriptional control of the interferon system

Khabar

Young

2007

Biochimie

Self Cite

View full text Add to dashboard Cite

The interferon (IFN) system is a well-controlled network of signaling, transcriptional, and posttranscriptional processes that orchestrate host defense against microbes. The IFN response comprises a multi-array of IFN-stimulated gene products that mediate a variety of biological processes designed to control infection and regulate specific immune responses. In this review, we focus on posttranscriptional mechanisms of gene regulation that occur during the course of IFN induction and during the response of cells to IFN. Post-transcriptional mechanisms involve different levels of regulation such as mRNA stability, alternative splicing, and translation. Such controls offer a fine tuning mechanism for efficient and rapid response and as a negative feedback control in IFN biosynthesis and response.

show abstract

Expressed Gene Clusters Associated with Cellular Sensitivity and Resistance Towards Anti-viral and Anti-proliferative Actions of Interferon

Cited by 36 publications

References 32 publications

The type I interferon system in systemic lupus erythematosus

The type I interferon system in systemic lupus erythematosus

Induction of the interferon response by siRNA is cell type– and duplex length–dependent

Post-transcriptional control of the interferon system

Contact Info

Product

Resources

About