ArticleThe Journal of biological chemistry2008
Functional and structural profiling of the human thrombopoietin gene promoter.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Defective binding of ETS1 and STAT4 due to a mutation in the promoter region ofHaematologica · 2023Article
- Novel THPO variant in hereditary thrombocytopenia: A potential candidate variant for predisposition to myeloid neoplasm.PloS one · 2022Article
- Lipopolysaccharide Stimulated the Migration of NIH3T3 Cells Through a Positive Feedback Between β-Catenin and COX-2.Frontiers in pharmacology · 2018Article
- Tissue-specific differences in the regulation of KIBRA gene expression involve transcription factor TCF7L2 and a complex alternative promoter system.Journal of molecular medicine (Berlin, Germany) · 2014Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human thrombopoietin (TPO) is involved in cardiovascular disease as it regulates megakaryocyte development and enhances platelet adhesion/aggregation. The THPO promoter structure is still controversial. By reverse transcription-PCR, we confirm that THPO transcription is cell line-dependently initiated at two alternative promoters, which we newly designated P1a and P1. We subsequently electrophoretically scanned and resequenced these portions in 95 and 57 patients with cardiovascular disease, respectively, and identified seven variants (-1450/del58bp, C-920T [rs2855306], A-622G, C-413T [rs885838], C+5A, G+115A, and C+135T). After subcloning of 1032 bp of THPO P1 in pGL3-basic vector, five molecular haplotypes (MolHaps1-5) were observed: [A(-622)-C(-413)-C(+5)-G(+115); wild type (wt)], [A(-622)-T(-413)-C(+5)-G(+115)], [G(-622)-T(-413)-C(+5)-G(+115)], [A(-622)-C(-413)-A(+5)-G(+115)], [A(-622)-C(-413)-C(+5)-A(+115)], and analyzed in reporter gene assays in HEK293T and HepG2 cells. MolHaps 2, 4, and 5 were significantly more active than wt (all p values < or =0.01) in HEK293T cells, MolHap3 exerted a substantial loss of promoter activity (p < 0.0001 in HEK293T and p < 0.01 in HepG2, compared with wt). Electrophoretic mobility shift assays revealed that A-622G and C-413T individually differed from MolHaps in their DNA-protein interaction patterns. Supershift and chromatin immunoprecipitation assays identified CCAAT/enhancer-binding protein delta as the binding protein exclusively for the -622A allelic portion.
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