ArticleMolecular and cellular biochemistry2007
Identification of the distinct promoters for the two transcripts of apoptosis related protein 3 and their transcriptional regulation by NFAT and NFkappaB.
Article in Molecular and cellular biochemistry, 2007. 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, 21 citations in OpenAlex.
- Functional characterization of all-trans retinoic acid-induced differentiation factor (ATRAID).FEBS open bio · 2023Article
- Ultrasound Assisted Exosomal Delivery of Tissue Responsive mRNA for Enhanced Efficacy and Minimized Off-Target Effects.Molecular therapy. Nucleic acids · 2020Article
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- FK-3000 isolated from Stephania delavayi Diels. inhibits MDA-MB-231 cell proliferation by decreasing NF-κB phosphorylation and COX-2 expression.International journal of oncology · 2015Article
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- Toad glandular secretions and skin extractions as anti-inflammatory and anticancer agents.Evidence-based complementary and alternative medicine : eCAM · 2014Review
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- NELL-1 binds to APR3 affecting human osteoblast proliferation and differentiation.FEBS letters · 2011Article
- Identification of Juxtanodin promoter and its transcriptional regulation during the ATRA-induced differentiation of C6 cells.Molecular and cellular biochemistry · 2011Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
APR3 (apoptosis related protein 3) is a novel gene highly conserved across species. Analysis of the data about APR3 available at GEO profiles revealed consistent and significant changes of APR3 expression level in certain developmental and inflammatory processes. Based on the search and analysis of all the submitted mRNA sequence, we postulated that the two transcripts may arise from separate promoter activities rather than previously assumed alternative splicing. Through reporter assay and PCR data, we identified the distinct promoters for the two transcripts of APR3. Furthermore, exogenous expression of a constitutively active mutant of transcription factor NFAT was able to enhance both the promoter activities of APR3. Sequential deletion of the promoter from the 5' side and mutation of the promoter suggested the functional NFAT binding sites might localize between -96 bp and -47 bp. In contrast, exogenous expression of a constitutively active mutant of the transcription factor NFkB inhibited APR3 transcription. Our data suggested that APR3 might be functionally important in certain processes under which NFAT and/or NFkappaB are/is activated.
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