Localization of the Human Stat6 Gene to Chromosome 12q13.3–q14.1, a Region Implicated in Multiple Solid Tumors

Patel, Bharvin K.R.; Keck, Catherine L.; O’Leary, Ryan S.; Popescu, Nicholas C.; LaRochelle, William J.

doi:10.1006/geno.1998.5436

Cited by 36 publications

(28 citation statements)

References 35 publications

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“…STAT6 promoter constructs (pBP78, pBP88, pBP86 11 ) of different sizes (5.6kb, 2.6kb and 1.1kb) were used to identify the minimal region necessary for maximal STAT6 transcription in Jurkat T cells. Consistent with a previous report, 11 our data indicated that the minimal STAT6 promoter pBP86 (1.1kb) had the strongest transcriptional activity (15-fold upregulation) after T-cell stimulation (see this article's Fig E3 in the Online Repository at www.jacionline.org). The largest promoter construct pBP78 (5.6 kb) led to a 5-fold increase in comparison with the pGL3-basic vector.…”

Section: Intron 2 Silences Stat6 Promoter Activitysupporting

confidence: 92%

An IgE-associated polymorphism in STAT6 alters NF-κB binding, STAT6 promoter activity, and mRNA expression

Schedel

Frei

Bieli

et al. 2009

Journal of Allergy and Clinical Immunology

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Section: Intron 2 Silences Stat6 Promoter Activitysupporting

confidence: 92%

An IgE-associated polymorphism in STAT6 alters NF-κB binding, STAT6 promoter activity, and mRNA expression

Schedel

Frei

Bieli

et al. 2009

Journal of Allergy and Clinical Immunology

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“…c-Sis/PDGF BB, v-Abl (Danial et al, 1995) and p190 Bcr ± Abl (Ilaria and Van Etten, 1996) were found to induce Stat6 activation. Elucidation of the human Stat6 genomic structure and mapping to chromosome 12q13.3 ± q14.1 suggested that Stat6 may participate in the development of some solid tumors (Patel et al, 1998a). We have recently shown that IL-4 a ects speci®c PDGF-mediated biological responses (Patel et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Consequences of Stat6 deletion on Sis/PDGF- and IL-4-induced proliferation and transcriptional activation in murine fibroblasts

et al. 1999

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“…The gene maps to 12q13.3-q14.1, encompasses over 19 kb and consists of 23 exons 19 . The first two and part of third exons belong to 5´UTR (untranslated region) and a large part of the last exon is untranslated as well (Fig.…”

Section: Structure Of the Stat6 And Its Productmentioning

confidence: 99%

“…The first (rs2598483) is located 77 bp upstream of CCAAT box, suggested to be an enhancer, and 1771 bp upstream of a prominent transcriptional initiation site. The second lies closer to the site of transcription initiation, 1216 bp upstream of it, and 474 bp downstream of the CCAAT box 19 . Although they are relatively close to the CCAAT box and therefore could putatively have impact on transcription activity of the gene, they were not associated with asthma, peripheral eosinophil cell count or total IgE level in the Caucasian population 40,48,49 .…”

Section: Polymorphisms In Stat6 -Ige Level and Asthmamentioning

confidence: 99%

STAT6 - polymorphisms, haplotypes and epistasis in relation to atopy and asthma

Godava¹,

Vrtěl²,

Vodička³

2013

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. STAT6 has an important role in the IL-4 / IL-13 signalling pathway. Genome -wide association studies have shown that particular polymorphism (SNP) or haplotype variants of STAT6 as well as epigenetic gene modifications are associated with IgE level and asthma in childhood. Methods. A review of the available literature was performed to map out the function and signalling pathway of STAT6, studies of STAT6 SNPs association with susceptibility to asthma and atopy, covering the years 1997 -2012 were summarized, and the value of epigenetic and epistatic influences on STAT6 and their relevance to the development of the studied phenotype (atopy or asthma) were determined. Results. There are 2 SNPs (rs71802646 and rs320411) with clinical association and proven functional effect on STAT6 expression. The effect of STAT6 SNPs cumulates in haplotypes and more potently during interaction with SNPs in the genes from the signalling pathway (IL4, IL4Ra, and IL13). Expression of STAT6 is also influenced by DNA methylation. Atopy is traditionally believed to be maternally inherited but there is one report about paternally overtransmitted STAT6 haplotype (TCA haplotype, built from rs324011, rs3024974 and rs4559 SNPs). Conclusions. STAT6 polymorphisms and their combinations have an important influence on IgE level and development of asthma. However, the interaction between SNPs in the IL-4 / IL-13 signalling pathway is of greater impact. Hypermethylation of the STAT6 promoter is also significant in the regulation of STAT6 expression and this fact opens possibilities for targeting therapy in asthma.

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Localization of the Human Stat6 Gene to Chromosome 12q13.3–q14.1, a Region Implicated in Multiple Solid Tumors

Cited by 36 publications

References 35 publications

An IgE-associated polymorphism in STAT6 alters NF-κB binding, STAT6 promoter activity, and mRNA expression

An IgE-associated polymorphism in STAT6 alters NF-κB binding, STAT6 promoter activity, and mRNA expression

Consequences of Stat6 deletion on Sis/PDGF- and IL-4-induced proliferation and transcriptional activation in murine fibroblasts

STAT6 - polymorphisms, haplotypes and epistasis in relation to atopy and asthma

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