ArticleCellular & molecular biology letters2010
ZNF300, a recently identified human transcription factor, activates the human IL-2Rβ promoter through the overlapping ZNF300/EGR1 binding site.
Article in Cellular & molecular biology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Prognostic signature composed of transcription factors accurately predicts the prognosis of gastric cancer patients.Cancer cell international · 2021Article
- KRAB-ZFP Transcriptional Regulators Acting as Oncogenes and Tumor Suppressors: An Overview.International journal of molecular sciences · 2021Review
- ZNF300 promotes chemoresistance and aggressive behaviour in non-small-cell lung cancer.Cell proliferation · 2020Article
- Sex differences in the late first trimester human placenta transcriptome.Biology of sex differences · 2018Article
- Blood and Intestine eQTLs from an Anti-TNF-Resistant Crohn's Disease Cohort Inform IBD Genetic Association Loci.Clinical and translational gastroenterology · 2016Article
- Overexpression of the human ZNF300 gene enhances growth and metastasis of cancer cells through activating NF-kB pathway.Journal of cellular and molecular medicine · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
ZNF300 was recently identified as a member of the human KRAB/C(2)H(2) zinc finger protein family. Little is known about the role of ZNF300 in human gene regulation networks. In this study, the DNA-binding property of ZNF300 was further analyzed. We found that the recombinant ZNF300 could bind to the binding site 5'-GCGGGGGCG-3' of Egr1, another member of the KRAB/C(2)H(2) zinc finger protein family. Similarly, recombinant Egr1 also showed a similar binding affinity to the ZNF300 binding site 5'-CTGGGGGCG-3'. Bioinformatics analysis revealed that there is an overlapping ZNF300/Egr1 binding site in the human IL-2Rβ promoter region, which was previously known to be recognized by endogenous Egr1. Electrophoretic mobility shift assays showed that endogenous ZNF300 could also bind to this site. A transient transfection assay revealed that both ZNF300 and Egr1 could transactivate the IL-2Rβ promoter, and that the activation was abrogated by a mutation of residues in the overlapping ZNF300/Egr1 binding site. Co-expression of ZNF300 and Egr1 led to enhanced IL-2Rβ promoter activity. Thus, ZNF300 is likely to be another regulator of the human IL-2Rβ promoter.
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