Publication:
Expression of Aquaporin-1, -2 and -4 in Mice with a Spontaneous Mutation Leading to Hydronephrosis

dc.contributor.authorS. Ampawongen_US
dc.contributor.authorA. Klincomhumen_US
dc.contributor.authorW. Likitsuntonwongen_US
dc.contributor.authorO. Singhaen_US
dc.contributor.authorT. Ketjareonen_US
dc.contributor.authorY. Panavechkijkulen_US
dc.contributor.authorK. M. Zawen_US
dc.contributor.authorK. Kengkoomen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-06-11T05:11:32Z
dc.date.available2018-06-11T05:11:32Z
dc.date.issued2012-05-01en_US
dc.description.abstractThis study investigates the expression of aquaporin-1, -2 and -4 in mice with a spontaneously-arising mutation that leads to hydronephrosis (ICR/Mlac-hydro mice). The mutant mice developed bilateral non-obstructive hydronephrosis without evidence of interstitial fibrosis or glomerulosclerosis. The mice had no abnormality in blood urea nitrogen or creatinine concentrations or in urine specific gravity. Despite the severity of the renal damage the mice grew and reproduced normally. Kidneys from the mutant mice had reduced expression of all three aquaporins compared with wild type mice. The reduction in aquaporin was proportional to the degree of hydronephrosis, but this change did not appear to be associated with disturbance of urinary function. © 2011.en_US
dc.identifier.citationJournal of Comparative Pathology. Vol.146, No.4 (2012), 332-337en_US
dc.identifier.doi10.1016/j.jcpa.2011.08.005en_US
dc.identifier.issn15323129en_US
dc.identifier.issn00219975en_US
dc.identifier.other2-s2.0-84859428515en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/14811
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84859428515&origin=inwarden_US
dc.subjectMedicineen_US
dc.subjectVeterinaryen_US
dc.titleExpression of Aquaporin-1, -2 and -4 in Mice with a Spontaneous Mutation Leading to Hydronephrosisen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84859428515&origin=inwarden_US

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