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• W2092337132 abstract "Cardiac hormones atrial and brain natriuretic peptides activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA), which plays a critical role in reduction of blood pressure and blood volume. Currently, the mechanisms responsible for regulating the Npr1 gene (coding for GC-A/NPRA) transcription are not well understood. The present study was conducted to examine the interactive roles of all-trans retinoic acid (ATRA), Ets-1, Sp1, and histone acetylation on the transcriptional regulation and function of the Npr1 gene. Deletion analysis of the Npr1 promoter and luciferase assays showed that ATRA enhanced a 16-fold Npr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner. As confirmed by gel shift and chromatin immunoprecipitation assays, ATRA enhanced the binding of both Ets-1 and Sp1 to the Npr1 promoter. The retinoic acid receptor α (RARα) was recruited by Ets-1 and Sp1 to form a transcriptional activator complex with their binding sites in the Npr1 promoter. Interestingly, ATRA also increased the acetylation of histones H3 and H4 and enhanced their recruitment to Ets-1 and Sp1 binding sites within the Npr1 promoter. Collectively, the present results demonstrate that ATRA regulates Npr1 gene transcription and GC activity of the receptor by involving the interactive actions of Ets-1, Sp1, and histone acetylation." @default.
• W2092337132 created "2016-06-24" @default.
• W2092337132 creator A5009520844 @default.
• W2092337132 creator A5013084644 @default.
• W2092337132 creator A5046112673 @default.
• W2092337132 creator A5056077743 @default.
• W2092337132 date "2010-11-01" @default.
• W2092337132 modified "2023-10-16" @default.
• W2092337132 title "Interactive Roles of Ets-1, Sp1, and Acetylated Histones in the Retinoic Acid-dependent Activation of Guanylyl Cyclase/Atrial Natriuretic Peptide Receptor-A Gene Transcription" @default.
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• W2092337132 doi "https://doi.org/10.1074/jbc.m110.132795" @default.
• W2092337132 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2988357" @default.
• W2092337132 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20864529" @default.
• W2092337132 hasPublicationYear "2010" @default.
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