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This study investigated how TAZ (a transcriptional coactivator with PDZ\u2010binding motif,\n                    <jats:italic>Wwtr1<\/jats:italic>\n                    ) controls vasopressin\u2010driven AQP2 expression. AQP2 expression was studied using collecting duct\u2010specific TAZ\u2010knockout (TAZ\n                    <jats:sup>f\/f<\/jats:sup>\n                    ; HoxB7Cre) mice and siRNA\u2010mediated knockdown of TAZ in vasopressin\u2010responsive mpkCCDc11 cells. Downstream factors of TAZ were identified using transcriptomics and bioinformatics. The TAZ\n                    <jats:sup>f\/f<\/jats:sup>\n                    ; HoxB7Cre mice demonstrated polyuria and a significant decrease in AQP2 abundance in the kidney cortex and the outer medulla. dDAVP treatment (10\n                    <jats:sup>\u22129<\/jats:sup>\n                    \u2009M, 24\u2009h) on mpkCCDc11 cells significantly increased AQP2 mRNA and protein levels. However, siRNA\u2010mediated TAZ knockdown (TAZ\u2010KD) markedly attenuated these effects without affecting cAMP levels. Immunocytochemical analysis revealed a substantial decrease in AQP2 immunolabeling intensity in TAZ\u2010KD cells following dDAVP stimulation. RNA sequencing analysis identified 1370 and 1985 differentially expressed genes in TAZ\u2010KD cells under basal conditions and after dDAVP treatment, respectively. Among 17 previously identified transcription factor (TF) candidates, seven (\n                    <jats:italic>Nr4a1, Cebpb, Mef2d, Elf3, Klf5, Junb, Stat3<\/jats:italic>\n                    ) were significantly upregulated by dDAVP in either control or TAZ\u2010KD conditions. Among them, RT\u2010qPCR analysis identified\n                    <jats:italic>Nr4a1<\/jats:italic>\n                    as a TAZ\u2010dependent TF, and immunoblotting revealed reduced NR4A1 protein levels in TAZ\u2010KD cells upon dDAVP stimulation. This finding suggests its role as a TAZ\u2010regulated target in dDAVP response pathway. Accordingly, Nr4a1\u2010KD reduced the dDAVP\u2010induced upregulation of\n                    <jats:italic>Aqp2<\/jats:italic>\n                    mRNA and protein. KEGG pathway enrichment analysis revealed that HIF\u20101 signaling and glycolysis as central pathways affected by TAZ. TAZ\u2010NR4A1 axis acts as a novel transcriptional regulatory mechanism in controlling vasopressin\u2010mediated AQP2 expression.\n                  <\/jats:p>","DOI":"10.1096\/fj.202500686rr","type":"journal-article","created":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T09:35:32Z","timestamp":1750930532000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Vasopressin\u2010Sensitive\n                    <i>Aqp2<\/i>\n                    Regulation Mediated by the\n                    <scp>TAZ<\/scp>\n                    \u2010\n                    <scp>NR4A1<\/scp>\n                    Axis in Renal Collecting Duct Cells"],"prefix":"10.1096","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2890-0006","authenticated-orcid":false,"given":"Hong Seok","family":"Choi","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Cell Biology Kyungpook National University  Taegu 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