ArticleThe Biochemical journal2003
The transcriptional repressor gene Mad3 is a novel target for regulation by E2F1.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Overexpression of MAX dimerization protein 3 (MXD3) predicts poor prognosis in clear cell renal cell carcinoma.Translational andrology and urology · 2021Article
- MXD3 as an Immunological and Prognostic Factor From Pancancer Analysis.Frontiers in molecular biosciences · 2021Article
- Alternative Splicing of MXD3 and Its Regulation of MXD3 Levels in Glioblastoma.Frontiers in molecular biosciences · 2019Article
- Novel targeted therapy for neuroblastoma: silencing the MXD3 gene using siRNA.Pediatric research · 2017Article
- MXD3 regulation of DAOY cell proliferation dictated by time course of activation.BMC cell biology · 2014Article
- Regulation of the MAD1 promoter by G-CSF.Nucleic acids research · 2008Article
- A novel role of the Mad family member Mad3 in cerebellar granule neuron precursor proliferation.Molecular and cellular biology · 2007Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mad family proteins are transcriptional repressors that antagonize the activity of the c- Myc proto-oncogene product. Mad3 is expressed specifically during the S-phase of the cell cycle in both proliferating and differentiating cells, suggesting that its biological function is probably linked to processes that occur during this period. To determine the mechanisms that regulate the cell-cycle-specific transcription of Mad3, we used reporter gene assays in stably transfected fibroblasts. We show that the activation of Mad3 at the G1-S boundary is mediated by a single E2F (E2 promoter binding factor)-binding site within the 5'-flanking region of the gene. Mutation of this element eliminated transcriptional activation at S-phase, suggesting that the positively acting E2F proteins play a role in Mad3 regulation. Using electrophoretic mobility-shift assays and chromatin immunoprecipitation, we show that E2F1 binds to the Mad3 5'-flanking region both in vitro and in vivo. We thus identify Mad3 as a novel transcriptional target of E2F1.
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