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High dietary inorganic phosphate affects lung through altering protein translation, cell cycle, and angiogenesis in developing mice

DC Field Value Language
dc.contributor.authorJin, Hua-
dc.contributor.authorChang, Seung-Hee-
dc.contributor.authorXu, Cheng-Xiong-
dc.contributor.authorShin, Ji-Young-
dc.contributor.authorChung, Youn-Sun-
dc.contributor.authorPark, Sung-Jin-
dc.contributor.authorLee, Yeon-Sook-
dc.contributor.authorAn, Gil-Hwan-
dc.contributor.authorLee, Kee-Ho-
dc.contributor.authorCho, Myung-Haing-
dc.date.accessioned2009-09-01-
dc.date.available2009-09-01-
dc.date.created2018-03-26-
dc.date.issued2007-11-
dc.identifier.citationToxicological Sciences, Vol.100 No.1, pp.215-223-
dc.identifier.issn1096-6080-
dc.identifier.other30302-
dc.identifier.urihttps://hdl.handle.net/10371/8339-
dc.description.abstractInorganic phosphate (Pi) plays a key role in diverse physiological functions. Several studies indicate that Pi may affect lung cell development through Na/Pi cotransporter (NPT). Several NPT subtypes have been identified in mammalian lung, and considerable progress has been made in our understanding of their function and regulation. Therefore, current study was performed to elucidate the potential effects of high dietary Pi on lungs of developing mice. Our results clearly demonstrate that high dietary Pi may affect the lung of developing mice through Akt-related cap-dependent protein translation, cell cycle regulation, and angiogenesis. Our results support the hypothesis that Pi works as a critical signal molecule for normal lung growth and suggest that careful restriction of Pi consumption may be important in maintaining a normal development.-
dc.language영어-
dc.language.isoenen
dc.publisherOxford University Press-
dc.titleHigh dietary inorganic phosphate affects lung through altering protein translation, cell cycle, and angiogenesis in developing mice-
dc.typeArticle-
dc.contributor.AlternativeAuthor조명행-
dc.identifier.doi10.1093/toxsci/kfm202-
dc.citation.journaltitleToxicological Sciences-
dc.identifier.wosid000250686600024-
dc.identifier.scopusid2-s2.0-35448984051-
dc.citation.endpage223-
dc.citation.number1-
dc.citation.startpage215-
dc.citation.volume100-
dc.identifier.sci000250686600024-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorLee, Yeon-Sook-
dc.contributor.affiliatedAuthorCho, Myung-Haing-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusSIGNALING PATHWAY-
dc.subject.keywordPlusMAMMALIAN TARGET-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordPlusHOMEOSTASIS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusPHOSPHORUS-
dc.subject.keywordPlusINITIATION-
dc.subject.keywordPlusRAPAMYCIN-
dc.subject.keywordPlusCALCIUM-
dc.subject.keywordAuthorAkt-
dc.subject.keywordAuthorprotein translation-
dc.subject.keywordAuthorcell cycle-
dc.subject.keywordAuthorangiogenesis-
dc.subject.keywordAuthorlung-
dc.subject.keywordAuthorinorganic phosphate-
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