May 15, 1996Biochemical JournalOpen Access

Transcriptional induction of the human renin gene by cyclic AMP requires cyclic AMP response element-binding protein (CREB) and a factor binding a pituitary-specific trans-acting factor (Pit-1) motif

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Population

Chorionic cells and kidney cortex cell nuclear extracts

Comparison

Forskolin treatment and promoter mutations vs Wild-type promoter constructs and untreated cells

Design

Preclinical

Authors

SGStéphane GermainCentre National de la Recherche Scientifique TKTadashi KonoshitaUniversity of Fukui JPJ.-M. PhilippeCommissariat à l'Énergie Atomique et aux Énergies Alternatives

Discussion

Member takes

Overview

Extends molecular mapping of renin promoter control; hypothesis-generating for cAMP pathways with no direct clinical translation yet.

Structured PICO

Population

Chorionic cells and kidney cortex cell nuclear extracts

Intervention

Forskolin treatment and promoter mutations (CRE and Pit-1 sites)

Comparator

Wild-type promoter constructs and untreated cells

Outcome

Luciferase reporter gene expression and protein-DNA binding (EMSAs, DNase I footprinting)surrogate

Maximal cAMP-induced transcription of the human renin gene requires both CREB binding to the CRE and distinct tissue-specific factors interacting with the Pit-1 motif.

Cite This Study

Germain et al. (1996) studied this question.

synapsesocial.com/papers/6a70f1be8031ec7bb1dcad42 https://doi.org/10.1042/bj3160107

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May 15, 1996Biochemical JournalOpen Access

Transcriptional induction of the human renin gene by cyclic AMP requires cyclic AMP response element-binding protein (CREB) and a factor binding a pituitary-specific trans-acting factor (Pit-1) motif

View Full Paper

Ask AI

Bookmark

Population

Chorionic cells and kidney cortex cell nuclear extracts

Comparison

Forskolin treatment and promoter mutations vs Wild-type promoter constructs and untreated cells

Design

Preclinical

Authors

SGStéphane GermainCentre National de la Recherche Scientifique TKTadashi KonoshitaUniversity of Fukui JPJ.-M. PhilippeCommissariat à l'Énergie Atomique et aux Énergies Alternatives

Discussion

Member takes

Overview

Extends molecular mapping of renin promoter control; hypothesis-generating for cAMP pathways with no direct clinical translation yet.

Structured PICO

Population

Chorionic cells and kidney cortex cell nuclear extracts

Intervention

Forskolin treatment and promoter mutations (CRE and Pit-1 sites)

Comparator

Wild-type promoter constructs and untreated cells

Outcome

Luciferase reporter gene expression and protein-DNA binding (EMSAs, DNase I footprinting)surrogate

Maximal cAMP-induced transcription of the human renin gene requires both CREB binding to the CRE and distinct tissue-specific factors interacting with the Pit-1 motif.

Cite This Study

Germain et al. (1996) studied this question.

synapsesocial.com/papers/6a70f1be8031ec7bb1dcad42 https://doi.org/10.1042/bj3160107

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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