ArticleGenes and immunity2013
Multiple sclerosis-associated single-nucleotide polymorphisms in CLEC16A correlate with reduced SOCS1 and DEXI expression in the thymus.
Article in Genes and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Risk variants disrupting enhancers of TProceedings of the National Academy of Sciences of the United States of America · 2019Trial
- Functional dissection of noncoding variants associated with rheumatoid arthritis.Annals of the rheumatic diseases · 2025Article
- Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025Review
- Review
- SOCS-JAK-STAT inhibitors and SOCS mimetics as treatment options for autoimmune uveitis, psoriasis, lupus, and autoimmune encephalitis.Frontiers in immunology · 2023Review
- Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences.Biomedicines · 2020Review
- The type 1 diabetes candidate gene Dexi does not affect disease risk in the nonobese diabetic mouse model.Genes and immunity · 2020Article
- The Genetic Contribution to Type 1 Diabetes.Current diabetes reports · 2019Review
- Mechanisms of gastrointestinal allergic disorders.The Journal of clinical investigation · 2019Review
- DEXI, a candidate gene for type 1 diabetes, modulates rat and human pancreatic beta cell inflammation via regulation of the type I IFN/STAT signalling pathway.Diabetologia · 2019Article
- Genetic-Driven Druggable Target Identification and Validation.Trends in genetics : TIG · 2018Review
- Suppressor of Cytokine Signaling (SOCS)1 Regulates Interleukin-4 (IL-4)-activated Insulin Receptor Substrate (IRS)-2 Tyrosine Phosphorylation in Monocytes and Macrophages via the Proteasome.The Journal of biological chemistry · 2016Article
- 5-Hydroxymethylcytosine Remodeling Precedes Lineage Specification during Differentiation of Human CD4(+) T Cells.Cell reports · 2016Article
- Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival.Scientific reports · 2016Article
- Systemic Lupus Erythematosus Patients Exhibit Reduced Expression of CLEC16A Isoforms in Peripheral Leukocytes.International journal of molecular sciences · 2015Article
- Multiple sclerosis-associated CLEC16A controls HLA class II expression via late endosome biogenesis.Brain : a journal of neurology · 2015Article
- Regulation of Macrophage, Dendritic Cell, and Microglial Phenotype and Function by the SOCS Proteins.Frontiers in immunology · 2015Review
- Multiple Sclerosis Risk Allele in CLEC16A Acts as an Expression Quantitative Trait Locus for CLEC16A and SOCS1 in CD4+ T Cells.PloS one · 2015Article
- Fine mapping and functional studies of risk variants for type 1 diabetes at chromosome 16p13.13.Diabetes · 2014Article
- Genome-wide association analysis identifies 11 risk variants associated with the asthma with hay fever phenotype.The Journal of allergy and clinical immunology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies have revealed that the 16p13 chromosomal region, including CLEC16A, DEXI, CIITA and SOCS1, is associated with susceptibility to autoimmune diseases. As non-coding single-nucleotide polymorphisms (SNPs) may confer susceptibility to disease by affecting expression of nearby genes, we examined whether autoimmune-associated intronic CLEC16A SNPs (rs12708716, rs6498169 and rs7206912) correlate with the expression of CLEC16A itself as well as neighboring genes in whole-blood and thymic samples. Real-time quantitative PCR analyses show that SOCS1 and DEXI expression was lower in thymic samples carrying at least one of the CLEC16A risk alleles compared with non-carriers of the risk allele. Linear regression analysis revealed a significant correlation between the expression level of CLEC16A and that of SOCS1 and DEXI in thymic samples. These data indicate a possible regulatory role for multiple sclerosis-associated non-coding CLEC16A SNPs and a common control mechanism for the expression of CLEC16A, SOCS1 and DEXI.
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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 OpenQuestion graph.