| http://purl.uniprot.org/citations/28405619 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28405619 | http://www.w3.org/2000/01/rdf-schema#comment | "Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6-/-) mice and potentially novel connecting tubule/principal cell-specific AC6 knockout (AC6loxloxCre) mice had approximately 50% lower urine osmolality and doubled water intake under baseline conditions compared with controls. Dietary Li+ administration increased water intake and reduced urine osmolality in control, AC6-/-, and AC6loxloxCre mice. Consistent with AC6-/- mice, medullary AQP2 and pS256-AQP2 abundances were lower in AC6loxloxCre mice compared with controls under standard conditions, and levels were further reduced after Li+ administration. AC6loxloxCre and control mice had a similar increase in the numbers of proliferating cell nuclear antigen-positive cells in response to Li+. However, AC6loxloxCre mice had a higher number of H+-ATPase B1 subunit-positive cells under standard conditions and after Li+ administration. Collectively, AC6 has a minor role in Li-NDI development but may be important for determining the intercalated cell-to-principal cell ratio."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci.insight.91042"xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Fenton R.A."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Kohan D.E."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Rieg T."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Brooks H.L."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Poulsen S.B."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/author | "Kristensen T.B."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/name | "JCI Insight"xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/pages | "e91042"xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/title | "Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus."xsd:string |
| http://purl.uniprot.org/citations/28405619 | http://purl.uniprot.org/core/volume | "2"xsd:string |
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