ArticleJournal of biomedical research2010
A novel SATB1 binding site in the BCL2 promoter region possesses transcriptional regulatory function.
Article in Journal of biomedical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 citing papers in PubMed, 6 citations in OpenAlex.
- Tumour suppressor EP300, a modulator of paclitaxel resistance and stemness, is downregulated in metaplastic breast cancer.Breast cancer research and treatment · 2017Article
- Effector bottleneck: microbial reprogramming of parasitized host cell transcription by epigenetic remodeling of chromatin structure.Frontiers in genetics · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
BCL2 is a key regulator of apoptosis. Our previous work has demonstrated that special AT-rich sequence-binding protein 1 (SATB1) is positively correlated with BCL2 expression. In the present study, we report a new SATB1 binding site located between P1 and P2 promoters of the BCL2 gene. The candidate SATB1 binding sequence predicted by bioinformatic analysis was investigated in vitro and in vivo by electrophoretic gel mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP). One 25-bp sequence, named SB1, was confirmed to be SATB1 binding site. The regulatory function of SB1 and its relevance to SATB1 were further examed with dual-luciferase reporter assay system in Jurkat cells. We found that SB1 could negatively regulate reporter gene activity. Mutation of SATB1 binding site further repressed the activity. Knockdown of SATB1 also enhanced this negative effect of SB1. Our data indicate that the SB1 sequence possesses negative transcriptional regulatory function and this function can be antagonized by SATB1.
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