ArticleJournal of cellular biochemistry2011
SUMOylation of DLX3 by SUMO1 promotes its transcriptional activity.
Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- SENP3 alleviates osteoporosis via promoting SIRT3 transcription through the increase of DLX2 stability via SUMO2/3.Cell biology and toxicology · 2025Article
- The miR-4739/DLX3 Axis Modulates Bone Marrow-Derived Mesenchymal Stem Cell (BMSC) Osteogenesis Affecting Osteoporosis Progression.Frontiers in endocrinology · 2021Article
- Steroidogenic Factor 1 (NR5A1) Activates ATF3 Transcriptional Activity.International journal of molecular sciences · 2020Article
- Roles of FoxM1 in cell regulation and breast cancer targeting therapy.Medical oncology (Northwood, London, England) · 2017Review
- SUMOylation of FOXM1B alters its transcriptional activity on regulation of MiR-200 family and JNK1 in MCF7 human breast cancer cells.International journal of molecular sciences · 2014Article
- Acidic residue Glu199 increases SUMOylation level of nuclear hormone receptor NR5A1.International journal of molecular sciences · 2013Article
- Loss of SUMOylation on ATF3 inhibits proliferation of prostate cancer cells by modulating CCND1/2 activity.International journal of molecular sciences · 2013Article
- Neural crest deletion of Dlx3 leads to major dentin defects through down-regulation of Dspp.The Journal of biological chemistry · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Small ubiquitin-like modifiers (SUMO) are post-translational modifiers that regulate target protein activity in diverse ways. The most common group of SUMO substrates is transcription factors, whose transcriptional activity can be altered positively or negatively as a result of SUMOylation. DLX3 is a homeodomain transcription factor involved in placental development, in the differentiation of structures involving epithelial-mesenchymal interactions, such as hair, teeth and nails, and in bone mineralization. We identified two potential SUMOylation sites in the N-terminal domain of DLX3 at positions K83 and K112. Among the six members of the Distal-less family, DLX3 is the only member containing these sites, which are highly conserved among vertebrates. Co-expression experiments demonstrated that DLX3 can be SUMOylated by SUMO1. Site-directed mutagenesis of lysines 83 and 112 to arginines (K83R and K112R) demonstrated that only K112 is involved in SUMOylation. Immunocytochemical analysis determined that SUMOylation does not affect DLX3 translocation to the nucleus and favors perinuclear localization. Moreover, using electrophoresis mobility shift assay (EMSA), we found that DLX3 is still able to bind DNA when SUMOylated. Using luciferase reporter assays, we showed that DLX3(K112R) exhibits a significantly lower transcriptional activity compared to DLX3(WT), suggesting that SUMOylation has a positive effect on DLX3 activity. We identified a new level of regulation in the activity of DLX3 that may play a crucial role in the regulation of hair, teeth, and bone development.
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