Recognition of interferon-inducible sites, promoters, and enhancers

Ananko, E. A.; Kondrakhin, Yury V.; Merkulova, T. I.; Колчанов, Н. А.

doi:10.1186/1471-2105-8-56

Cited by 14 publications

(4 citation statements)

References 22 publications

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“…Based on the RANTES promoter region [26] , [34] , IRF-1 was identified as a proximal transcription factor and the increases in TNFα- or IL-1β-induced in nuclear IRF-1 levels were analyzed by western blotting [ Figure 6A ]. In these experiments the IRF-1 levels on western blots were quantified by densitomery and IRF-1 levels were calculated as a fold change from nuclear IRF-1 densitometry from control cells.…”

Section: Resultsmentioning

confidence: 99%

Hyperosmolarity Invokes Distinct Anti-Inflammatory Mechanisms in Pulmonary Epithelial Cells: Evidence from Signaling and Transcription Layers

et al. 2014

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Hypertonic saline (HTS) has been used intravenously to reduce organ dysfunction following injury and as an inhaled therapy for cystic fibrosis lung disease. The role and mechanism of HTS inhibition was explored in the TNFα and IL-1β stimulation of pulmonary epithelial cells. Hyperosmolar (HOsm) media (400 mOsm) inhibited the production of select cytokines stimulated by TNFα and IL-1β at the level of mRNA translation, synthesis and release. In TNFα stimulated A549 cells, HOsm media inhibited I-κBα phosphorylation, NF-κB translocation into the nucleus and NF-κB nuclear binding. In IL-1β stimulated cells HOsm inhibited I-κBα phosphorylation without affecting NF-κB translocation or nuclear binding. Incubation in HOsm conditions inhibited both TNFα and IL-1β stimulated nuclear localization of interferon response factor 1 (IRF-1). Additional transcription factors such as AP-1, Erk-1/2, JNK and STAT-1 were unaffected by HOsm. HTS and sorbitol supplemented media produced comparable outcomes in all experiments, indicating that the effects of HTS were mediated by osmolarity, not by sodium. While not affecting MAPK modules discernibly in A549 cells, both HOsm conditions inhibit IRF-1 against TNFα or IL-1β, but inhibit p65 NF-kB translocation only against TNFα but not IL-1β. Thus, anti-inflammatory mechanisms of HTS/HOsm appear to disrupt cytokine signals at distinct intracellular steps.

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Section: Resultsmentioning

confidence: 99%

Hyperosmolarity Invokes Distinct Anti-Inflammatory Mechanisms in Pulmonary Epithelial Cells: Evidence from Signaling and Transcription Layers

et al. 2014

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“…A number of Stat1- and ISGF3-binding sites were predicted for each sequence part. We decided to concentrate on the homologous sequence part nearest to the transcription start site (-161 to -637) of Oct-6 , based on a report showing that the regions -500 bp upstream of the transcription start site of IFN-inducible genes are enriched in predicted binding sites for Stat1 and ISGF3 [ 63 ].…”

Section: Methodsmentioning

confidence: 99%

Octamer-binding factor 6 (Oct-6/Pou3f1) is induced by interferon and contributes to dsRNA-mediated transcriptional responses

et al. 2010

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BackgroundOctamer-binding factor 6 (Oct-6, Pou3f1, SCIP, Tst-1) is a transcription factor of the Pit-Oct-Unc (POU) family. POU proteins regulate key developmental processes and have been identified from a diverse range of species. Oct-6 expression is described to be confined to the developing brain, Schwann cells, oligodendrocyte precursors, testes, and skin. Its function is primarily characterised in Schwann cells, where it is required for correctly timed transition to the myelinating state. In the present study, we report that Oct-6 is an interferon (IFN)-inducible protein and show for the first time expression in murine fibroblasts and macrophages.ResultsOct-6 was induced by type I and type II IFN, but not by interleukin-6. Induction of Oct-6 after IFNβ treatment was mainly dependent on signal transducer and activator of transcription 1 (Stat1) and partially on tyrosine kinase 2 (Tyk2). Chromatin immunopreciptitation experiments revealed binding of Stat1 to the Oct-6 promoter in a region around 500 bp upstream of the transcription start site, a region different from the downstream regulatory element involved in Schwann cell-specific Oct-6 expression. Oct-6 was also induced by dsRNA treatment and during viral infections, in both cases via autocrine/paracrine actions of IFNα/β. Using microarray and RT-qPCR, we furthermore show that Oct-6 is involved in the regulation of transcriptional responses to dsRNA, in particular in the gene regulation of serine/threonine protein kinase 40 (Stk40) and U7 snRNA-associated Sm-like protein Lsm10 (Lsm10).ConclusionOur data show that Oct-6 expression is not as restricted as previously assumed. Induction of Oct-6 by IFNs and viruses in at least two different cell types, and involvement of Oct-6 in gene regulation after dsRNA treatment, suggest novel functions of Oct-6 in innate immune responses.

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“…IFN-γ tarafından düzenlenen 200'den fazla gen bilinmektedir. Bu genlerdeki mutasyonlar viral, bakteriyel, paraziter ve bazı otoimmün hastalıklara karşı duyarlılığı artırabilmektedir 23,24 . IFN-γ +874 genetik varyantların HCV enfeksiyonunda klinik seyri etkileyebileceği, genotip ve alel faklılıkları ile polimorfizmler arasındaki etkileşimlerin ise HCV enfeksiyonunu kronikleşme veya sponton klirens yönünde değiştirebileceği belirtilmektedir [25][26][27] .…”

Section: Il-12a Ve Il-12b Genlerinde Bulunan çEşitli Hastalıklarla Ilişkili Olabilecek Snp'ler [Il-12bunclassified

TNF-α, IL-12A, IL-12B ve IFN-γ Gen Polimorfizmleri ile Kronik Hepatit C Arasındaki İlişkinin Araştırılması

Börekçi¹,

Çetinkaya²,

Kandemir³

et al. 2020

Mikrobiyol Bul

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Recognition of interferon-inducible sites, promoters, and enhancers

Cited by 14 publications

References 22 publications

Hyperosmolarity Invokes Distinct Anti-Inflammatory Mechanisms in Pulmonary Epithelial Cells: Evidence from Signaling and Transcription Layers

Hyperosmolarity Invokes Distinct Anti-Inflammatory Mechanisms in Pulmonary Epithelial Cells: Evidence from Signaling and Transcription Layers

Octamer-binding factor 6 (Oct-6/Pou3f1) is induced by interferon and contributes to dsRNA-mediated transcriptional responses

TNF-α, IL-12A, IL-12B ve IFN-γ Gen Polimorfizmleri ile Kronik Hepatit C Arasındaki İlişkinin Araştırılması

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