Vasopressin-induced water reabsorption by the renal collecting ducts is in part regulated by aquaporin-2 gene expression; however, the mechanism is not completely understood. We used genomic locus proteomics (GLoPro) to identify transcription protein network in the aquaporin-2 5’-flanking region in the mpkCCD cell model. Our strategy relied on a recombinant protein consisted of catalytic dead Cas9 and biotin ligase TurboID (dCas9-TurboID). When guided to -95 bp upstream to the aquaporin-2 transcription start site, it did not affect vasopressin analog dDAVP-induced aquaporin-2 gene transcription. The dCas9-TurboID was used to biotinylate proteins recruited by dDAVP to the above genomic region before affinity-purification followed by label-free identification and quantification with LC-MS/MS. In three independent experiments, 1,647 and 1,676 proteins were identified respectively in the vehicle and dDAVP-treated cells. Bioinformatics analysis showed enriched cellular component GO terms: nucleus, nucleoplasm, and nucleolus, consistent with functions of these identified proteins in gene regulation. Statistical analysis showed up-regulation of 310 proteins and down-regulation of 254 proteins in response to dDAVP. Biological process GO term analysis showed enrichment for mRNA processing, RNA splicing, and chromatin organization. In the dDAVP-upregulated group, we identified proteins involved in chromatin remodeling and histone modification that adjust chromatin accessibility: Baz2b, Npm3, Cbx8, Cdk17, Meaf6, and Prmt1. We also identified transcription factors and cofactors: Paxbp1, Rbm14, Cxxc1, Rbpms, Ccar1, Chch2, and JunB. Of these, JunB has been implicated in aquaporin-2 gene transcription. Based on prior omics data, we used Bayes’ theorem to rank these proteins for possibility in aquaporin-2 gene transcription. The top candidate was Ccar1, which is known to complex with β-catenin and T cell factor to enhance target gene transcription. Vasopressin induces β-catenin nuclear translocation; T cell factor has a conserved binding element in the aquaporin-2 5’-flanking region. Further study is needed to examine the possibility that Ccar1 involves β-catenin and T cell factor to regulate aquaporin-2 transcription. This research was supported by National Science and Technology Concil, R.O.C. (MOST111-2320-B-002-084-MY3). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.