ArticleMolecular biology reports2014
DNA methyltransferase 1(DNMT1) induced the expression of suppressors of cytokine signaling3 (Socs3) in a mouse model of asthma.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Structural and Functional Studies on Key Epigenetic Regulators in Asthma.Biomolecules · 2025Review
- Epigenetics and Asthma: A Systematic Review.Cureus · 2024Review
- Cyanocobalamin prevents cardiomyopathy in type 1 diabetes by modulating oxidative stress and DNMT-SOCS1/3-IGF-1 signaling.Communications biology · 2021Article
- Early-life exposure to three size-fractionated ultrafine and fine atmospheric particulates in Beijing exacerbates asthma development in mature mice.Particle and fibre toxicology · 2018Article
- Reg3g Promotes Pancreatic Carcinogenesis in a Murine Model of Chronic Pancreatitis.Digestive diseases and sciences · 2015Article
- Methylation and microRNA-mediated epigenetic regulation of SOCS3.Molecular biology reports · 2015Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNMT1 is the most important methyltransferase enzyme, involved in the regulation of gene expression and appropriate histone modification. It interact with proliferating cell nuclear antigen (PCNA), SNF2 family member ATP-dependent chromatin remodeling enzyme, cyclin dependent kinases inhibitor, E2F1 transcription factor and HDACs to form a repressor complex known as HDAC complexes. The interaction of DNMT1 with numerous protein suppressors of promoters suggests that the enzyme is a crucial element of the transcription suppression complex. Since the mechanism behind over expression of Socs3 in Asthma is unclear, we study the Epigenetic mode of overexpression of Socs3 in terms of methylation/acetylation/inactivation of HDACs/activation of HATs enzymes in a mouse model of asthma. The results show that low expression of DNMT1 might indirectly induce the expression of Socs3 and HAT, and inhibit the expression of HDACs family. Furthermore knockdown of DNMT1 by siRNA induced expression of Socs3 while knock down of Socs3 by siRNA has no effect on DNMT1 expression. Our result suggests that the over expression of Socs3 is due to the inhibition of HDACs complex and hyperacetylation of histones molecule along with down regulation of DNMT1 gene. In depth study on DNMT1 might be useful for the development of therapeutic drug against asthma/allergic diseases.
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