Promoter analysis of interleukin 19

Chen, Po‐Jen; Wei, Chang-Ching; Wang, Chihuei; Chen, Feng Wei; Hsu, Yu Feng; Chang, Ming Shi

doi:10.1016/j.bbrc.2006.03.200

Cited by 10 publications

(9 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For both genes, the lowest basal promoter activity was observed with the longest promoter fragment tested but activity increased significantly with 5′ truncation suggesting the presence of binding sites for transcriptional repressors in the upstream region. Previous studies reported that deletion of the 5′ upstream region was a prerequisite for mapping the activation sites in the proximal promoters of the interleukin 19 and fucosyltransferase VI genes (Chen et al, 2006; Higai et al, 2008). Upstream sites that repress the transcriptional activation by TFs binding to TFBSs in the proximal promoter region were also previously identified in the promoters of genes for which transcription is known to be tightly regulated (Garban and Bonavida, 2001; Lindas and Tomkinson, 2007).…”

Section: Discussionmentioning

confidence: 99%

Activation of Oas1a gene expression by type I IFN requires both STAT1 and STAT2 while only STAT2 is required for Oas1b activation

2012

View full text Add to dashboard Cite

The murine 2′-5′ oligoadenylate synthetase 1a (Oas1a) and Oas1b genes are type 1 IFN responsive genes. Oas1a is an active synthetase with broad antiviral activity mediated through RNase L. Oas1b is inactive but can inhibit Oas1a synthetase activity and mediate a flavivirus-specific antiviral activity through an unknown RNase L-independent mechanism. Analysis of promoter elements regulating gene transcription confirmed that an IFN-stimulated response element (ISRE) is required for IFN beta-activation but neither the overlapping IRF binding site present in both promoters nor the adjacent Oas1b NF-kappa B site is required. Mutation of the overlapping STAT site negatively affected IFN beta-induction of Oas1a but not of Oas1b. Also, IFN beta induction of Oas1a was STAT1- and STAT2-dependent, while induction of Oas1b was STAT1-independent but STAT2-dependent. The two promoters differ at a single nucleotide in the STAT site. The data indicate that these two duplicated genes can be differentially regulated by IFN beta.

show abstract

Section: Discussionmentioning

confidence: 99%

Activation of Oas1a gene expression by type I IFN requires both STAT1 and STAT2 while only STAT2 is required for Oas1b activation

2012

View full text Add to dashboard Cite

show abstract

“…Different lengths of IL‐19 promoter–luciferase reporters were generated using the sticky end PCR cloning technique . The human genomic BAC clone (BACPAC Resource Center Oakland, California; clone ID: RP11‐237C22) contains the IL‐19 promoter sequence described previously . The fragments were cloned into the Kpn I and Hin dIII sites of the pGL3‐Enhancer Vector (Promega, Madison, WI).…”

Section: Methodsmentioning

confidence: 99%

“…35 The human genomic BAC clone (BACPAC Resource Center Oakland, California; clone ID: RP11-237C22) contains the IL-19 promoter sequence described previously. 36 The fragments were cloned into the KpnI and HindIII sites of the pGL3-Enhancer Vector (Promega, Madison, WI). The primers used in the subcloning are listed in Table 1.…”

Section: Generation Of the Il-19 Promoter-luciferase Constructsmentioning

confidence: 99%

Interleukin‐4 up‐regulation of epidermal interleukin‐19 expression in keratinocytes involves the binding of signal transducer and activator of transcription 6 (Stat6) to the imperfect Stat6 sites

et al. 2014

View full text Add to dashboard Cite

Summary Interleukin‐19 (IL‐19) plays an important role in asthma by stimulating T helper type 2 (Th2) cytokine production. Interestingly, IL‐4, a key Th2 cytokine, in turn up‐regulates IL‐19 expression in bronchial epithelial cells, so forming a positive feedback loop. In atopic dermatitis (AD), another Th2 disease closely related to asthma, IL‐19 is up‐regulated in the skin. We propose to use IL‐4 transgenic (Tg) mice and human keratinocyte culture to delineate the molecular mechanisms involved in the up‐regulation of IL‐19 in AD. IL‐19 is similarly up‐regulated in the skin of IL‐4 Tg mice as in human AD. Next we show that IL‐4 up‐regulates IL‐19 expression in keratinocytes. Interestingly, the up‐regulation was suppressed by a pan‐Janus kinase (Jak) inhibitor, suggesting that the Jak–signal transducer and activator of transcription (Jak‐STAT) pathway may be involved. Dominant negative studies further indicate that STAT6, but not other STATs, mediates the up‐regulation. Serial 5′ deletion of the IL‐19 promoter and mutagenesis studies demonstrate that IL‐4 up‐regulation of IL‐19 in keratinocytes involves two imperfect STAT6 response elements. Finally, chromatin immunoprecipitation assay studies indicate that IL‐4 increases the binding of STAT6 to its response elements in the IL‐19 promoter. Taken together, we delineate the detailed molecular pathway for IL‐4 up‐regulation of IL‐19 in keratinocytes, which may play an important role in AD pathogenesis.

show abstract

“…Certain studies have indicated that any change in the sequence TGTGGT (À142 to À138) abolishes IL-19 promoter activity, which acts as the binding site for the transcription factors [21]. Results of Yamamoto and colleagues [22] suggested that IL-19 polymorphisms (rs2243188 and rs2243193) might have a protective role in the progress of ulcerative colitis in Mexican patients.…”

Section: Il-19mentioning

confidence: 95%

IL-19 and IL-20 genes polymorphisms and haplotype analysis in a vesicoureteral reflux population

2013

View full text Add to dashboard Cite

Promoter analysis of interleukin 19

Cited by 10 publications

References 15 publications

Activation of Oas1a gene expression by type I IFN requires both STAT1 and STAT2 while only STAT2 is required for Oas1b activation

Activation of Oas1a gene expression by type I IFN requires both STAT1 and STAT2 while only STAT2 is required for Oas1b activation

Interleukin‐4 up‐regulation of epidermal interleukin‐19 expression in keratinocytes involves the binding of signal transducer and activator of transcription 6 (Stat6) to the imperfect Stat6 sites

IL-19 and IL-20 genes polymorphisms and haplotype analysis in a vesicoureteral reflux population

Contact Info

Product

Resources

About