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dc.contributor.author오영석-
dc.date.accessioned2018-04-15T15:25:44Z-
dc.date.available2018-04-15T15:25:44Z-
dc.date.issued2012-05-
dc.identifier.citationAndrologia, Vol.44, No.S1 [2012], p383-389en_US
dc.identifier.issn0303-4569-
dc.identifier.urihttp://onlinelibrary.wiley.com/doi/abs/10.1111/j.1439-0272.2011.01195.x-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/67046-
dc.description.abstractVitamin B12 (cobalamin) deficiency results in atrophy of seminiferous tubules and aplasia of spermatozoa and spermatid. The transmembrane protein amnionless (AMN) directs endocytosis of cubilin with its ligand, contributing to intrinsic factor-vitamin B12 absorption. To understand vitamin B12 transport in testis, we analysed AMN expression in developing mouse testes and in Leydig cells and speculated the possible role of AMN in testis. In testes, Amn mRNA levels were low until 14 days post partum ( pp) and markedly increased from puberty onwards. In the interstitium, Amn mRNA levels were low at 14 days pp and increased at puberty (28 days pp) together with 3-beta-hydroxysteroid dehydrogenase type 6 mRNA. Strong AMN immunoreactivity was observed in early spermatocytes from 7 days pp, suggesting that AMN participates in meiosis. In Leydig cells, AMN was not observed until 14 days pp but was strongly expressed after 28 days pp, suggesting a positive relationship between AMN expression and functional differentiation of adult Leydig cells. Together, AMN may participate in meiosis in early spermatocytes and in functional differentiation of adult Leydig cells through the mediation of vitamin B12 transport in the mouse testes. This is the first report on AMN expression in the germ cells and soma of mammalian testes.en_US
dc.description.sponsorshipThis work was supported by KRF.en_US
dc.language.isoenen_US
dc.publisherBlackwell Publishing Ltden_US
dc.subjectAmnionlessen_US
dc.subjectgerm cellsen_US
dc.subjectLeydig cellsen_US
dc.subjectmouse testesen_US
dc.subjectvitamin B12en_US
dc.titleExpression of amnionless in mouse testes and Leydig cellsen_US
dc.typeArticleen_US
dc.relation.noSuppl 1-
dc.relation.volume44-
dc.identifier.doi10.1111/j.1439-0272.2011.01195.x-
dc.relation.page383-389-
dc.relation.journalANDROLOGIA-
dc.contributor.googleauthorOh, Y. S.-
dc.contributor.googleauthorPark, H. Y.-
dc.contributor.googleauthorGye, M. C.-
dc.relation.code2012200608-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentTHE RESEARCH INSTITUTE FOR NATURAL SCIENCES-
dc.identifier.pidysoh2001-
dc.identifier.researcherID55434029200-
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