{"entity": "journal", "iuid": "bd4a2e042e494b1a9bc20e785c6b2c93", "timestamp": "2026-06-08T06:02:28.496Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Exp.%20Dermatol..json"}, "display": {"href": "https://publications.scilifelab.se/journal/Exp.%20Dermatol."}}, "title": "Exp. Dermatol.", "issn": "1600-0625", "issn-l": "0906-6705", "publications_count": 2, "publications": [{"entity": "publication", "iuid": "c8f5dbcb52864b11a987807b315f87ed", "links": {"self": {"href": "https://publications.scilifelab.se/publication/c8f5dbcb52864b11a987807b315f87ed.json"}, "display": {"href": "https://publications.scilifelab.se/publication/c8f5dbcb52864b11a987807b315f87ed"}}, "title": "RNA Sequencing Reveals the Long Non-Coding RNA Signature in Psoriasis Keratinocytes and Identifies CYDAER as a Long Non-Coding RNA Regulating Epidermal Differentiation.", "authors": [{"family": "Freisenhausen", "given": "Jan Cedric", "initials": "JC", "orcid": "0000-0002-3078-0365", "researcher": {"href": "https://publications.scilifelab.se/researcher/74f596e44f3d4dd78d499469c9f0b04e.json"}}, {"family": "Luo", "given": "Longlong", "initials": "L", "orcid": "0000-0002-5931-0666", "researcher": {"href": "https://publications.scilifelab.se/researcher/aa6310dd902342b4a74bac1efd4090c0.json"}}, {"family": "Kelemen", "given": "Evelyn", "initials": "E", "orcid": "0000-0002-8357-790X", "researcher": {"href": "https://publications.scilifelab.se/researcher/8f1c75b553304176b8cafa84815421e8.json"}}, {"family": "Elton", "given": "Jonathan", "initials": "J", "orcid": "0000-0003-4919-8065", "researcher": {"href": "https://publications.scilifelab.se/researcher/22bf1246696541abafd2c2ad902a3b84.json"}}, {"family": "Skoog", "given": "Viktor", "initials": "V", "orcid": "0009-0005-8862-1534", "researcher": {"href": "https://publications.scilifelab.se/researcher/160d22c12c9743e193a47f6ded86b7ad.json"}}, {"family": "Pivarcsi", "given": "Andor", "initials": "A", "orcid": "0000-0003-2196-1102", "researcher": {"href": "https://publications.scilifelab.se/researcher/77ca870317234573a3da5dffb24bb268.json"}}, {"family": "Sonkoly", "given": "Enik\u00f6", "initials": "E", "orcid": "0000-0002-4909-5413", "researcher": {"href": "https://publications.scilifelab.se/researcher/5c1ce318445d4b2bb586ac1f8ed8ed87.json"}}], "type": "journal article", "published": "2025-02-00", "journal": {"title": "Exp. Dermatol.", "issn": "1600-0625", "volume": "34", "issue": "2", "pages": "e70054", "issn-l": "0906-6705"}, "abstract": "Psoriasis is a common chronic inflammatory skin disease determined by genetic and environmental factors, resulting in the activation of IL-23/IL-17-mediated immune response, epidermal hyperproliferation, and keratinocyte activation. Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts > 500 nucleotides with diverse regulatory functions; their role in epidermal dysfunction in psoriasis is poorly understood. To identify epidermal transcripts with potential roles in psoriasis, including lncRNAs, we performed RNA sequencing on keratinocytes from psoriasis and healthy skin. We identified 889 differentially expressed lncRNAs, many of which with yet unknown functions. RP11-295G20.2 was identified as a lncRNA significantly induced in psoriasis keratinocytes, and this was verified by qRT-PCR and by single-molecule in situ hybridisation. Analysis of subcellular fractions of epidermis revealed a cytoplasmic localisation in line with results of single molecule in situ hybridisation. We report that RP11-295G20.2 has a skin-enriched expression, and within skin it is mainly expressed in suprabasal epidermal layers. Moreover, RP11-295G20.2 is induced by the key psoriasis cytokine IL-17A and shows a dynamic regulation during keratinocyte differentiation with upregulation during early differentiation and downregulation in the late stage. Knockdown of RP11-295G20.2 in keratinocytes promotes terminal differentiation. Based on our findings, we named RP11-295G20.2 Cytoplasmic Differentiation-Associated Epidermal RNA, CYDAER. In summary, our study provides a comprehensive characterisation of the non-coding RNA landscape of psoriasis keratinocytes and identifies CYDAER as a skin-enriched lncRNA regulating keratinocyte differentiation. Our data suggest that overexpression of CYDAER may contribute to altered differentiation in psoriatic epidermis.", "doi": "10.1111/exd.70054", "pmid": "39953783", "labels": {"NGI Short read": "Service", "NGI Uppsala (SNP&SEQ Technology Platform)": "Service", "National Genomics Infrastructure": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC11829188"}], "notes": [], "created": "2025-09-08T06:52:12.448Z", "modified": "2025-09-08T06:52:13.267Z"}, {"entity": "publication", "iuid": "5ff4e71e15e44069813db0fafb8c6d30", "links": {"self": {"href": "https://publications.scilifelab.se/publication/5ff4e71e15e44069813db0fafb8c6d30.json"}, "display": {"href": "https://publications.scilifelab.se/publication/5ff4e71e15e44069813db0fafb8c6d30"}}, "title": "Genome-wide association study identifies new susceptibility loci for cutaneous lupus erythematosus.", "authors": [{"family": "Kunz", "given": "Manfred", "initials": "M"}, {"family": "K\u00f6nig", "given": "Inke R", "initials": "IR"}, {"family": "Schillert", "given": "Arne", "initials": "A"}, {"family": "Kruppa", "given": "Jochen", "initials": "J"}, {"family": "Ziegler", "given": "Andreas", "initials": "A"}, {"family": "Grallert", "given": "Harald", "initials": "H"}, {"family": "M\u00fcller-Nurasyid", "given": "Martina", "initials": "M"}, {"family": "Lieb", "given": "Wolfgang", "initials": "W"}, {"family": "Franke", "given": "Andre", "initials": "A"}, {"family": "Ranki", "given": "Annamari", "initials": "A"}, {"family": "Panelius", "given": "Jaana", "initials": "J"}, {"family": "Koskenmies", "given": "Sari", "initials": "S"}, {"family": "Hasan", "given": "Taina", "initials": "T"}, {"family": "Kere", "given": "Juha", "initials": "J"}, {"family": "R\u00f6nn", "given": "Ann-Charlotte", "initials": "AC"}, {"family": "Simon", "given": "Jan C", "initials": "JC"}, {"family": "Schmidt", "given": "Enno", "initials": "E"}, {"family": "Wenzel", "given": "Joerg", "initials": "J"}, {"family": "T\u00fcting", "given": "Thomas", "initials": "T"}, {"family": "Landsberg", "given": "Jennifer", "initials": "J"}, {"family": "Zeller", "given": "Tanja", "initials": "T"}, {"family": "Blankenberg", "given": "Stefan", "initials": "S"}, {"family": "Gl\u00e4ser", "given": "Regine", "initials": "R"}, {"family": "Patsinakidis", "given": "Nikolaos", "initials": "N"}, {"family": "Kuhn", "given": "Annegret", "initials": "A"}, {"family": "Ibrahim", "given": "Saleh M", "initials": "SM"}], "type": "journal article", "published": "2015-07-00", "journal": {"volume": "24", "issn": "1600-0625", "issue": "7", "pages": "510-515", "title": "Exp. Dermatol.", "issn-l": "0906-6705"}, "abstract": "Cutaneous lupus erythematosus (CLE) is a chronic autoimmune disease of the skin with typical clinical manifestations. Here, we genotyped 906\u00a0600 single nucleotide polymorphisms (SNPs) in 183 CLE cases and 1288 controls of Central European ancestry. Replication was performed for 13 SNPs in 219 case subjects and 262 controls from Finland. Association was particularly pronounced at 4 loci, all with genomewide significance (P\u00a0<\u00a05\u00a0\u00d7\u00a010(-8) ): rs2187668 (PGWAS \u00a0=\u00a01.4\u00a0\u00d7\u00a010(-12) ), rs9267531 (PGWAS \u00a0=\u00a04.7\u00a0\u00d7\u00a010(-10) ), rs4410767 (PGWAS \u00a0=\u00a01.0\u00a0\u00d7\u00a010(-9) ) and rs3094084 (PGWAS \u00a0=\u00a01.1\u00a0\u00d7\u00a010(-9) ). All mentioned SNPs are located within the major histocompatibility complex (MHC) region of chromosome 6 and near genes of known immune functions or associations with other autoimmune diseases such as HLA-DQ alpha chain 1 (HLA-DQA1), MICA, MICB, MSH5, TRIM39 and RPP21. For example, TRIM39/RPP21 read through transcript is a known mediator of the interferon response, a central pathway involved in the pathogenesis of CLE and systemic lupus erythematosus (SLE). Taken together, this genomewide analysis of disease association of CLE identified candidate genes and genomic regions that may contribute to pathogenic mechanisms in CLE via dysregulated antigen presentation (HLA-DQA1), apoptosis regulation, RNA processing and interferon response (MICA, MICB, MSH5, TRIM39 and RPP21).", "doi": "10.1111/exd.12708", "pmid": "25827949", "labels": {"Mutation Analysis Facility (MAF)": null}, "xrefs": [], "notes": [], "created": "2017-05-02T12:57:40.408Z", "modified": "2017-05-30T13:11:11.155Z"}], "created": "2017-05-09T09:12:28.905Z", "modified": "2020-11-27T13:14:05.986Z"}