The activation of specific gene expression programs of immune cells contributes to inflammation and inflammatory diseases. Gene expression program can be regulated on both the transcriptional and posttranscriptional levels. Transcriptional regulation includes epigenetic mechanisms involving methylation and modification of DNA and RNA molecules, histone modifications, non-coding RNAs and 3D chromatin architectures. For example, the key cis-regulatory element for transcriptional activation via physical contact with promoter is enhancer. Moreover, their physical contact is orchestrated by higher-chromatin structures called insulated neighborhoods. Pre-mRNA splicing in addition to transcriptional control, is a fundamental process required for expression control in human cells. Alternative splicing of pre-mRNA enables a gene to generate multiple distinct mRNA transcripts and protein isoforms with altered biological functions. Dysregulation in alternative splicing has been implicated in many inflammatory diseases, including Crohn's disease. Hence, uncovering the molecular mechanisms of transcriptional and posttranscriptional regulation in inflammatory diseases will provide novel insights into disease pathogenesis and identify potential therapeutic targets.
This Special Issue aims to publish high-quality original articles and review articles that provide novel insights and conceptual advancements in epigenetic and transcriptional regulation in inflammation, including the regulatory hierarchies from nucleotide sequences to 3D chromatin architecture and transcriptional heterogeneity of immune cell subsets in inflammatory disease. We kindly encourage all research groups covering relevant areas within the issue’s scope to contribute up-to-date, full-length articles, highlighting the latest developments in their research field, or to invite relevant experts and colleagues to do so.
1. Chromatin dynamics in inflammation and inflammatory disease.
2. 3D genomic control of transcription in inflammation and inflammatory disease.
3. Alternative splicing in inflammatory disease.
The activation of specific gene expression programs of immune cells contributes to inflammation and inflammatory diseases. Gene expression program can be regulated on both the transcriptional and posttranscriptional levels. Transcriptional regulation includes epigenetic mechanisms involving methylation and modification of DNA and RNA molecules, histone modifications, non-coding RNAs and 3D chromatin architectures. For example, the key cis-regulatory element for transcriptional activation via physical contact with promoter is enhancer. Moreover, their physical contact is orchestrated by higher-chromatin structures called insulated neighborhoods. Pre-mRNA splicing in addition to transcriptional control, is a fundamental process required for expression control in human cells. Alternative splicing of pre-mRNA enables a gene to generate multiple distinct mRNA transcripts and protein isoforms with altered biological functions. Dysregulation in alternative splicing has been implicated in many inflammatory diseases, including Crohn's disease. Hence, uncovering the molecular mechanisms of transcriptional and posttranscriptional regulation in inflammatory diseases will provide novel insights into disease pathogenesis and identify potential therapeutic targets.
This Special Issue aims to publish high-quality original articles and review articles that provide novel insights and conceptual advancements in epigenetic and transcriptional regulation in inflammation, including the regulatory hierarchies from nucleotide sequences to 3D chromatin architecture and transcriptional heterogeneity of immune cell subsets in inflammatory disease. We kindly encourage all research groups covering relevant areas within the issue’s scope to contribute up-to-date, full-length articles, highlighting the latest developments in their research field, or to invite relevant experts and colleagues to do so.
1. Chromatin dynamics in inflammation and inflammatory disease.
2. 3D genomic control of transcription in inflammation and inflammatory disease.
3. Alternative splicing in inflammatory disease.