A new mouse strain manifesting high proteinuria and Kidney glomerular defect

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dc.contributor.authorByung Hwa Hyun-
dc.contributor.authorN Wakasugi-
dc.contributor.authorM Nose-
dc.contributor.authorT Saito-
dc.contributor.authorT Tomita-
dc.date.accessioned2017-04-19T08:44:05Z-
dc.date.available2017-04-19T08:44:05Z-
dc.date.issued1991-
dc.identifier.issn0023-6764-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/3162-
dc.description.abstractA mutant strain of mice manifesting high proteinuria, wasting syndrome, and kidney glomerular defect was established from the F5 offspring of an interstrain cross of CBA/Nga and RFM/Nga mice. Affected mice had high levels of proteinuria after 40 days of age. The body weight of about 22.6% of affected mice decreased rapidly and they died between 3 and 5 months of age. We learned that this abnormality is controlled by two pairs of autosomal recessive genes; the mutant strain of mice is designated FGS/Nga. The mutant strain has been characterized by high proteinuria and renal lesions with focal sclerosis of glomeruli and tubular atrophy with interstitial nephritis in the kidney resembling the human disease. The FGS/Nga mouse strain is a potential animal model for studying kidney glomerular defect in humans.-
dc.publisherUnknown-
dc.titleA new mouse strain manifesting high proteinuria and Kidney glomerular defect-
dc.title.alternativeA new mouse strain manifesting high proteinuria and Kidney glomerular defect-
dc.typeArticle-
dc.citation.titleLaboratory Animal Science-
dc.citation.number5-
dc.citation.endPage446-
dc.citation.startPage442-
dc.citation.volume41-
dc.contributor.affiliatedAuthorByung Hwa Hyun-
dc.contributor.alternativeName현병화-
dc.contributor.alternativeNameWakasugi-
dc.contributor.alternativeNameNose-
dc.contributor.alternativeNameSaito-
dc.contributor.alternativeNameTomita-
dc.identifier.bibliographicCitationLaboratory Animal Science, vol. 41, no. 5, pp. 442-446-
dc.description.journalClassN-
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