ArticleBMC biology2020
Mapping DNA interaction landscapes in psoriasis susceptibility loci highlights KLF4 as a target gene in 9q31.
Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Genomic loci and molecular genetic mechanisms for hidradenitis suppurativa.The British journal of dermatology · 2025Pooled it
- Harnessing Natural Compounds in Psoriasis: Targeting Cellular Pathways for Effective Therapy.Phytotherapy research : PTR · 2026Review
- HNRNPU and architectural lncRNAs as nuclear tethers of epithelial state stability.EMBO molecular medicine · 2026Review
- High-resolution promoter interaction analysis implicates genes involved in the activation of Type 3 Innate Lymphoid Cells in autoimmune disease risk.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic reprogramming in autoimmune and immune-mediated skin disease.Frontiers in immunology · 2026Review
- Psoriasis risk allele function in activated Th1/17 cells with "memory" to antigen exposure.PloS one · 2026Article
- The Genetic Background of Ankylosing Spondylitis Reveals a Distinct Overlap with Autoimmune Diseases: A Systematic Review.Journal of clinical medicine · 2025Review
- Multi-omics analysis in primary T cells elucidates mechanisms behind disease-associated genetic loci.Genome biology · 2025Article
- KLF feedback loops in innate immunity.Frontiers in immunology · 2025Review
- Functional Genomics in Psoriasis.International journal of molecular sciences · 2024Review
- Disentangling the complexity of psoriasis in the post-genome-wide association era.Genes and immunity · 2023Review
- A Review of CRISPR-Based Advances in Dermatological Diseases.Molecular diagnosis & therapy · 2023Review
- Multi-Omics Research Strategies for Psoriasis and Atopic Dermatitis.International journal of molecular sciences · 2023Review
- A global high-density chromatin interaction network reveals functional long-range and trans-chromosomal relationships.Genome biology · 2022Article
- Psoriasis: An Immunogenetic Perspective.Global medical genetics · 2022Review
- Skin Barrier Dysregulation in Psoriasis.International journal of molecular sciences · 2021Review
- Transcriptional enhancers and their communication with gene promoters.Cellular and molecular life sciences : CMLS · 2021Review
- Detecting chromosomal interactions in Capture Hi-C data with CHiCAGO and companion tools.Nature protocols · 2021Article
- Chromatin Looping Links Target Genes with Genetic Risk Loci for Dermatological Traits.The Journal of investigative dermatology · 2021Article
- Transcriptional and signalling regulation of skin epithelial stem cells in homeostasis, wounds and cancer.Experimental dermatology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundGenome-wide association studies (GWAS) have uncovered many genetic risk loci for psoriasis, yet many remain uncharacterised in terms of the causal gene and their biological mechanism in disease. This is largely a result of the findings that over 90% of GWAS variants map outside of protein-coding DNA and instead are enriched in cell type- and stimulation-specific gene regulatory regions.
resultsHere, we use a disease-focused Capture Hi-C (CHi-C) experiment to link psoriasis-associated variants with their target genes in psoriasis-relevant cell lines (HaCaT keratinocytes and My-La CD8+ T cells). We confirm previously assigned genes, suggest novel candidates and provide evidence for complexity at psoriasis GWAS loci. For one locus, uniquely, we combine further epigenomic evidence to demonstrate how a psoriasis-associated region forms a functional interaction with the distant (> 500 kb) KLF4 gene. This interaction occurs between the gene and active enhancers in HaCaT cells, but not in My-La cells. We go on to investigate this long-distance interaction further with Cas9 fusion protein-mediated chromatin modification (CRISPR activation) coupled with RNA-seq, demonstrating how activation of the psoriasis-associated enhancer upregulates KLF4 and its downstream targets, relevant to skin cells and apoptosis.
conclusionsThis approach utilises multiple functional genomic techniques to follow up GWAS-associated variants implicating relevant cell types and causal genes in each locus; these are vital next steps for the translation of genetic findings into clinical benefit.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.