April 1, 1994Journal of Clinical InvestigationOpen Access

Molecular mechanism of transcriptional activation of angiotensinogen gene by proximal promoter.

Q: What is the clinical evidence from this study?

Study design: Other. Population: Hypertension (pathogenesis context). Intervention: Angiotensinogen proximal promoter constructs vs. Promoterless or mutated constructs. Primary outcome: HepG2-specific CAT activity.

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Key result

The proximal promoter region from -96 to +22 of the transcriptional start site, through synergistic interplay between AGF2 and AGF3, is essential for HepG2-specific angiotensinogen promoter activation.

Population

Hepatoma cell line HepG2, cervical carcinoma HeLa cells, glioblastoma T98G cells, embryonic fibroblast…

Comparison

5'-deleted constructs of the angiotensinogen… vs Promoterless plasmid pUCSV0CAT, pUCSV3CAT, and…

Design

Preclinical

Authors

KTKouichi TamuraGeneral Cardiology SUS UmemuraKyoto Prefectural University of Medicine MIMasao IshiiNihon University

Discussion

Member takes

Implication

Maps minimal angiotensinogen promoter in vitro; leaves open its relevance to hypertension pathogenesis.

Structured PICO

Population

Hepatoma cell line HepG2, cervical carcinoma HeLa cells, glioblastoma T98G cells, embryonic fibroblast NIH3T3 cells, and C57BL/6 mouse liver extracts

Intervention

5'-deleted constructs of the angiotensinogen gene promoter linked to chloramphenicol acetyltransferase (CAT) gene, and site-directed mutagenesis of AGE2 or AGE3

Comparator

Promoterless plasmid pUCSV0CAT (negative control), pUCSV3CAT (positive control), and unmutated wild-type constructs

Outcome

Transcriptional activation measured by CAT activity, and DNA-protein complex formation measured by electrophoretic mobility shift assay (EMSA) and DNase I footprintingsurrogate

The synergistic interplay between liver-specific nuclear factor AGF2 and ubiquitous nuclear factor AGF3 on the proximal promoter is essential for the transcriptional activation of the angiotensinogen gene.

Cite This Study

Tamura et al. (1994) studied Hypertension (pathogenesis context). Angiotensinogen proximal promoter constructs vs. Promoterless or mutated constructs was evaluated on HepG2-specific CAT activity. The proximal promoter region from -96 to +22 of the transcriptional start site, through synergistic interplay between AGF2 and AGF3, is essential for HepG2-specific angiotensinogen promoter activation.

synapsesocial.com/papers/6a6a85c845e10bb5bcf2bdef https://doi.org/10.1172/jci117113

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April 1, 1994Journal of Clinical InvestigationOpen Access

Molecular mechanism of transcriptional activation of angiotensinogen gene by proximal promoter.

View Full Paper

Ask AI

Bookmark

Key result

Population

Hepatoma cell line HepG2, cervical carcinoma HeLa cells, glioblastoma T98G cells, embryonic fibroblast…

Comparison

5'-deleted constructs of the angiotensinogen… vs Promoterless plasmid pUCSV0CAT, pUCSV3CAT, and…

Design

Preclinical

Authors

KTKouichi TamuraGeneral Cardiology SUS UmemuraKyoto Prefectural University of Medicine MIMasao IshiiNihon University

Discussion

Member takes

Implication

Maps minimal angiotensinogen promoter in vitro; leaves open its relevance to hypertension pathogenesis.

Structured PICO

Population

Hepatoma cell line HepG2, cervical carcinoma HeLa cells, glioblastoma T98G cells, embryonic fibroblast NIH3T3 cells, and C57BL/6 mouse liver extracts

Intervention

5'-deleted constructs of the angiotensinogen gene promoter linked to chloramphenicol acetyltransferase (CAT) gene, and site-directed mutagenesis of AGE2 or AGE3

Comparator

Promoterless plasmid pUCSV0CAT (negative control), pUCSV3CAT (positive control), and unmutated wild-type constructs

Outcome

Transcriptional activation measured by CAT activity, and DNA-protein complex formation measured by electrophoretic mobility shift assay (EMSA) and DNase I footprintingsurrogate

Cite This Study

synapsesocial.com/papers/6a6a85c845e10bb5bcf2bdef https://doi.org/10.1172/jci117113

Also Consider

Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context:

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