ArticleNucleic acids research2011
Discovery of SMAD4 promoters, transcription factor binding sites and deletions in juvenile polyposis patients.
Article in Nucleic acids research, 2011. 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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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Dysregulation of transcripts SMAD4-209 and SMAD4-213 and their respective promoters in colon cancer cell lines.Journal of Cancer · 2024Article
- Interaction of C/EBPβ with SMAD2 and SMAD4 genes induces the formation of lipid droplets in bovine myoblasts.Functional & integrative genomics · 2023Article
- SMAD4-201 transcript as a putative biomarker in colorectal cancer.BMC cancer · 2022Article
- Molecular Characterization and Functional Analysis of Two Steroidogenic Genes TSPO and SMAD4 in Yellow Catfish.International journal of molecular sciences · 2021Article
- Co-Expression Network Analysis Identifies miRNA⁻mRNA Networks Potentially Regulating Milk Traits and Blood Metabolites.International journal of molecular sciences · 2018Article
- Roles of Smads Family and Alternative Splicing Variants of Smad4 in Different Cancers.Journal of Cancer · 2018Review
- ConBind: motif-aware cross-species alignment for the identification of functional transcription factor binding sites.Nucleic acids research · 2016Article
- Unveiling combinatorial regulation through the combination of ChIP information and in silico cis-regulatory module detection.Nucleic acids research · 2012Article
- A review of integration strategies to support gene regulatory network construction.TheScientificWorldJournal · 2012Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Inactivation of SMAD4 has been linked to several cancers and germline mutations cause juvenile polyposis (JP). We set out to identify the promoter(s) of SMAD4, evaluate their activity in cell lines and define possible transcription factor binding sites (TFBS). 5'-rapid amplification of cDNA ends (5'-RACE) and computational analyses were used to identify candidate promoters and corresponding TFBS and the activity of each was assessed by luciferase vectors in different cell lines. TFBS were disrupted by site-directed mutagenesis (SDM) to evaluate the effect on promoter activity. Four promoters were identified, two of which had significant activity in several cell lines, while two others had minimal activity. In silico analysis revealed multiple potentially important TFBS for each promoter. One promoter was deleted in the germline of two JP patients and SDM of several sites led to significant reduction in promoter activity. No mutations were found by sequencing this promoter in 65 JP probands. The predicted TFBS profiles for each of the four promoters shared few transcription factors in common, but were conserved across several species. The elucidation of these promoters and identification of TFBS has important implications for future studies in sporadic tumors from multiple sites, and in JP patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.