Dataset Information


ChIP-Seq analysis of Histone H3 acetylation (K27) changes in response to vasopressin in mouse renal collecting duct mpkCCD cells

ABSTRACT: In mammals, the peptide hormone vasopressin controls renal water excretion, largely through regulation of the molecular water channel aquaporin-2 (AQP2) in the renal collecting duct. Regulatory mechanisms of AQP2 show: 1) short-term regulation by membrane trafficking; and 2) long-term regulation involving vasopressin-induced changes in the abundance of the aquaporin-2 protein. Vasopressin activates a G protein-coupled receptor (V2R) increasing cyclic AMP and activating protein kinase PKA. Crebbp and Ep300 are known targets of PKA. They are histone acetyltransferases that acetylate histone H3 lysine-27, a histone mark associated with open chromatin and increased transcription (Tie F et al. Development 2009). The translocation of CREBBP and Ep300 into the nucleus in response to vasopressin in the collecting duct cells, predicts that vasopressin, working through PKA, may increase histone H3K27 acetylation of some genes. We tested this by performing ChIP-Seq for this modification. Overall design: To identify changes of Histone modification (acetylation) in response to vasopressin in cultured mouse collecting duct cells (mpkCCD), we carried out ChIP-seq for genome-wide distribution of histone 3 acetylation (H3K27ac) (n=2). Observations were made both after 24-hr treatment with the vasopressin analog dDAVP and with vehicle.

INSTRUMENT(S): Illumina HiSeq 2000 (Mus musculus)

SUBMITTER: Hyun Jun Jung  

PROVIDER: GSE95007 | GEO | 2018-01-02



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Systems-level identification of PKA-dependent signaling in epithelial cells.

Isobe Kiyoshi K   Jung Hyun Jun HJ   Yang Chin-Rang CR   Claxton J'Neka J   Sandoval Pablo P   Burg Maurice B MB   Raghuram Viswanathan V   Knepper Mark A MA  

Proceedings of the National Academy of Sciences of the United States of America 20171002 42

G protein stimulatory α-subunit (Gαs)-coupled heptahelical receptors regulate cell processes largely through activation of protein kinase A (PKA). To identify signaling processes downstream of PKA, we deleted both PKA catalytic subunits using CRISPR-Cas9, followed by a "multiomic" analysis in mouse kidney epithelial cells expressing the Gαs-coupled V2 vasopressin receptor. RNA-seq (sequencing)-based transcriptomics and SILAC (stable isotope labeling of amino acids in cell culture)-based quantita  ...[more]

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