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Article: Aldose reductase-deficient mice develop nephrogenic diabetes insipidus

TitleAldose reductase-deficient mice develop nephrogenic diabetes insipidus
Authors
Ho, HTBChung, SKLaw, JWSKo, BCBTam, SCFBrooks, HLKnepper, MAChung, SSM
Issue Date2000
PublisherAmerican Society for Microbiology.
Citation
Molecular and Cellular Biology, 2000, v. 20 n. 16, p. 5840-5846 How to Cite?
DOI: http://dx.doi.org/10.1128/MCB.20.16.5840-5846.2000
AbstractAldose reductase (ALR2) is thought to be involved in the pathogenesis of various diseases associated with diabetes mellitus, such as cataract, retinopathy, neuropathy, and nephropathy. However, its physiological functions are not well understood. We developed mice deficient in this enzyme and found that they had no apparent developmental or reproductive abnormality except that they drank and urinated significantly more than their wild-type littermates. These ALR2-deficient mice exhibited a partially defective urine-concentrating ability, having a phenotype resembling that of nephrogenic diabetes insipidus.
Persistent Identifierhttp://hdl.handle.net/10722/48965
ISSN
0270-7306
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.452
PubMed Central ID
PMC86061
ISI Accession Number ID
WOS:000088524200006
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorHo, HTBen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorLaw, JWSen_HK
dc.contributor.authorKo, BCBen_HK
dc.contributor.authorTam, SCFen_HK
dc.contributor.authorBrooks, HLen_HK
dc.contributor.authorKnepper, MAen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2008-06-12T06:30:56Z-
dc.date.available2008-06-12T06:30:56Z-
dc.date.issued2000en_HK
dc.identifier.citationMolecular and Cellular Biology, 2000, v. 20 n. 16, p. 5840-5846en_HK
dc.identifier.issn0270-7306en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48965-
dc.description.abstractAldose reductase (ALR2) is thought to be involved in the pathogenesis of various diseases associated with diabetes mellitus, such as cataract, retinopathy, neuropathy, and nephropathy. However, its physiological functions are not well understood. We developed mice deficient in this enzyme and found that they had no apparent developmental or reproductive abnormality except that they drank and urinated significantly more than their wild-type littermates. These ALR2-deficient mice exhibited a partially defective urine-concentrating ability, having a phenotype resembling that of nephrogenic diabetes insipidus.en_HK
dc.format.extent384 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology.en_HK
dc.relation.ispartofMolecular and Cellular Biologyen_HK
dc.subject.meshAldehyde Reductase - deficiency - geneticsen_HK
dc.subject.meshDiabetes Insipidus, Nephrogenic - etiology - genetics - metabolismen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshMiceen_HK
dc.titleAldose reductase-deficient mice develop nephrogenic diabetes insipidusen_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1128/MCB.20.16.5840-5846.2000en_HK
dc.identifier.pmid10913167-
dc.identifier.pmcidPMC86061en_HK
dc.identifier.scopuseid_2-s2.0-0033859766en_HK
dc.identifier.hkuros113844-
dc.identifier.hkuros53084-
dc.identifier.hkuros69010-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033859766&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue16en_HK
dc.identifier.spage5840en_HK
dc.identifier.epage5846en_HK
dc.identifier.isiWOS:000088524200006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, HTB=55202560700en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridLaw, JWS=7202548738en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK
dc.identifier.scopusauthoridTam, SCF=7202037323en_HK
dc.identifier.scopusauthoridBrooks, HL=7102229699en_HK
dc.identifier.scopusauthoridKnepper, MA=35478273500en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.issnl0270-7306-

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