ArticleThe Biochemical journal2011
CpG methylation at the USF-binding site mediates cell-specific transcription of human ascorbate transporter SVCT2 exon 1a.
Article in The Biochemical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- The role of methylation in pituitary neuroendocrine tumors current insights and emerging perspectives.Molecular biology reports · 2026Review
- Molecular mechanism(s) involved in differential expression of vitamin C transporters along the intestinal tract.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Mechanism(S) Involved in the Colon-Specific Expression of the Thiamine Pyrophosphate (Tpp) Transporter.PloS one · 2016Article
- MicroRNAs-141 and 200a regulate the SVCT2 transporter in bone marrow stromal cells.Molecular and cellular endocrinology · 2015Article
- Methylation levels of SLC23A2 and NCOR2 genes correlate with spinal muscular atrophy severity.PloS one · 2015Article
- Article
- The vitamin C transporter SVCT2 is down-regulated during postnatal development of slow skeletal muscles.Histochemistry and cell biology · 2013Article
- Human genetic variation influences vitamin C homeostasis by altering vitamin C transport and antioxidant enzyme function.Annual review of nutrition · 2013Review
- DNA methylation analyses of urothelial carcinoma reveal distinct epigenetic subtypes and an association between gene copy number and methylation status.Epigenetics · 2012Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
SVCT2 (sodium-vitamin C co-transporter 2) is the major transporter mediating vitamin C uptake in most organs. Its expression is driven by two promoters (CpG-poor exon 1a promoter and CpG-rich exon 1b promoter). In the present study, we mapped discrete elements within the proximal CpG-poor promoter responsible for exon 1a transcription. We identified two E boxes for USF (upstream stimulating factor) binding and one Y box for NF-Y (nuclear factor Y) binding. We show further that NF-Y and USF bind to the exon 1a promoter in a co-operative manner, amplifying the binding of each to the promoter, and is absolutely required for the full activity of the exon 1a promoter. The analysis of the CpG site located at the upstream USF-binding site in the promoter showed a strong correlation between expression and demethylation. It was also shown that exon 1a transcription was induced in cell culture treated with the demethylating agent decitabine. The specific methylation of this CpG site impaired both the binding of USF and the formation of the functional NF-Y-USF complex as well as promoter activity, suggesting its importance for cell-specific transcription. Thus CpG methylation at the upstream USF-binding site functions in establishing and maintaining cell-specific transcription from the CpG-poor SVCT2 exon 1a promoter.
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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.