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DC Field | Value | Language |
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dc.citation.endPage | 28105 | - |
dc.citation.number | 42 | - |
dc.citation.startPage | 28095 | - |
dc.citation.title | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.volume | 283 | - |
dc.contributor.author | Hasler, Udo | - |
dc.contributor.author | Leroy, Valeeie | - |
dc.contributor.author | Jeon, Un Sil | - |
dc.contributor.author | Bouley, Richard | - |
dc.contributor.author | Dimitrov, Mitko | - |
dc.contributor.author | Kim, Jeong Ah | - |
dc.contributor.author | Brown, Dennis | - |
dc.contributor.author | Kwon, H. Moo | - |
dc.contributor.author | Martin, Pierre-Yves | - |
dc.contributor.author | Feraille, Eric | - |
dc.date.accessioned | 2023-12-22T08:36:40Z | - |
dc.date.available | 2023-12-22T08:36:40Z | - |
dc.date.created | 2014-06-02 | - |
dc.date.issued | 2008-10 | - |
dc.description.abstract | Renal tubulo-interstitial inflammation is frequently associated with polyuria and urine concentration defects. This led us to investigate the effects of the major pro-inflammatory nuclear factor kappa B (NF-kappa B) pathway on aquaporin 2 (AQP2) expression by the collecting duct. Using immortalized collecting duct principal cells (mpkCCD(c14)), we found that, acting independently of vasopressin, activation of NF-kappa B by lipopolysaccharide (LPS) decreased AQP2 mRNA and protein levels in a time-and dose-dependent manner but did not decrease AQP2 mRNA stability. Consistently, constitutively active I kappa B kinase beta decreased AQP2 expression. The LPS-induced decrease in AQP2 mRNA levels was confirmed in rat kidney slices and was reproduced both under conditions of elevated cAMP concentration and V-2 receptor antagonism. Computer analysis of the AQP2 promoter revealed two putative kappa B elements. Mutation of either kappa B element abolished the LPS-induced decrease of luciferase activity in cells expressing AQP2 promoter-luciferase plasmid constructs. Chromatin immunoprecipitation revealed that LPS challenge decreased p65, increased p50 and p52, and had no effect on RelB and c-Rel binding to kappa B elements of the AQP2 promoter. RNA-mediated interference silencing of p65, p50, and p52 confirmed controlled AQP2 transcription by these NF-kappa B subunits. We additionally found that hypertonicity activated NF-kappa B in mpkCCD(c14) cells, an effect that may counteract the Tonicity-responsive enhancer binding protein (TonEBP)-dependent increase in AQP2 gene transcription. Taken together, these findings indicate that NF-kappa B is an important physiological regulator of AQP2 transcription. | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.283, no.42, pp.28095 - 28105 | - |
dc.identifier.doi | 10.1074/jbc.M708350200 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.scopusid | 2-s2.0-57649136392 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/4847 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=57649136392 | - |
dc.identifier.wosid | 000259969300012 | - |
dc.language | 영어 | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
dc.title | NF-kappa B modulates aquaporin-2 transcription in renal collecting duct principal cells | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | INDUCED NEPHROTIC SYNDROME | - |
dc.subject.keywordPlus | ENHANCER-BINDING PROTEIN | - |
dc.subject.keywordPlus | WATER CHANNEL EXPRESSION | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | NULL MICE | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | HYPERTONICITY | - |
dc.subject.keywordPlus | PERMEABILITY | - |
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