ArticleGenes and immunity2007
Selective matrix attachment regions in T helper cell subsets support loop conformation in the Ifng gene.
Article in Genes and immunity, 2007. 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, 15 citations in OpenAlex.
- Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases.Frontiers in immunology · 2017Review
- Epigenetic control of cytokine gene expression: regulation of the TNF/LT locus and T helper cell differentiation.Advances in immunology · 2013Review
- Epigenetics and T helper 1 differentiation.Immunology · 2009Review
- Reconfiguration of genomic anchors upon transcriptional activation of the human major histocompatibility complex.Genome research · 2008Article
- Anchoring the genome.Genome biology · 2008Review
- Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Cytokine genes undergo progressive changes in chromatin organization when naïve CD4+ T helper (Th) cells differentiate into committed Th1 and Th2 lineages. Here, we analyzed nuclear matrix attachment regions (MARs) in the Ifng gene by DNA array technique in unactivated and activated CD4+ Th cells. This approach was combined with analysis of spatial organization of the Ifng gene by chromosome conformation capture approach to assess the relationship between the gene conformation and matrix attachment organization in functionally different cell subsets. We report that the Ifng gene in unactivated cells displays a linear conformation, but in T-cell receptor-activated cells, it adopts a loop conformation. The selective MARs support the spatial gene organization and characteristically define the Ifng gene in functionally different cell subsets. The pattern of interaction of the Ifng gene with the nuclear matrix dynamically changes in a lineage-specific manner in parallel with the changes in Ifng gene conformation. The data suggest that such structural dynamics provide the means for transcriptional regulation of the Ifng gene in the course of activation and differentiation of CD4+Th cells.
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Registered trials
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