Basic information of SLFN12 :
| Official Symbol of Gene | SLFN12 |
| Species | Homo sapiens |
| Entrez Gene ID | 55106 |
| Official Full Name | schlafen family member 12 |
| Also known as | SLFN3 |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSG00000172123 MIM:614955; AllianceGenome:HGNC:25500 |
| Map Location | 17q12 |
| Variation Type | methylation |
| refSNP ID | N/A |
Sample information of multiple sclerosis:
| Detected Sample | peripheral blood |
| Sample Detail | N/A |
| Detected Method | Illumina BeadChips |
| Disease | MS |
| Disease subtype | RRMS |
| Population | Norwegian,Australian |
| Sample Size | 94 cases / 94 healthy controls |
Literature information of multiple sclerosis :
| Pubmed ID | 30379917 |
| Year | 2018 |
| Title | Increased DNA methylation of SLFN12 in CD4+ and CD8+ T cells from multiple sclerosis patients |
Results of multiple sclerosis :
| Risk Type | Disease risk |
| Main Result | Positive |
| Result | A long DMR covering the first exon of SLFN12 showed hypermethylation in MS patients compared to healthy controls in both CD4+ and CD8+ T cells. Hypermethylation was seen in all strata, regardless of treatment status of cases. |
| Mechanism/Pathway | SLFN12 encodes a member of the Schlafen protein family, which is a family of proteins encoded by a cluster of five genes on chromosome 17.Type I IFNs induce the expression of Schlafen genes.SLFN12 has been shown to be downregulated during T-cell activation in primary human cells. From clinical observations and genetic studies,there is convincing evidence that MS pathology is driven by T-cells, and IFN beta type I is an approved therapy for MS, making SLFN12 a biologically plausible gene of interest for MS. |
