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dc.contributor.authorKoca, Ebru
dc.contributor.authorHaznedaroglu, Ibrahim C.
dc.contributor.authorAcar, Kadir
dc.contributor.authorBeyazit, Yavuz
dc.contributor.authorAksu, Salih
dc.contributor.authorMisirlioglu, Muge
dc.contributor.authorTuncer, Serdar
dc.contributor.authorSayinalp, Nilgun
dc.contributor.authorOzcebe, Osman I.
dc.contributor.authorUner, Aysegul
dc.date.accessioned2019-12-10T11:20:22Z
dc.date.available2019-12-10T11:20:22Z
dc.date.issued2007
dc.identifier.issn1470-3203
dc.identifier.urihttps://doi.org/10.3317/jraas.2007.019
dc.identifier.urihttp://hdl.handle.net/11655/15319
dc.description.abstractLocal renin-angiotensin system (RAS) may affect leukaemic cell production within the bone marrow microenvironment. Angiotensin-converting enzyme (ACE), renin, and angiotensin could influence leukaemogenesis. In this study, mRNA expressions of the major RAS components (ACE, renin, and angiotensinogen) in K562 human erythroleukaemia cell line have been searched by Real Time quantitative polymerase chain reaction. K562 blasts are multipotential, haematopoietic malignant cells that spontaneously differentiate into recognisable progenitors of the erythrocyte, granulocyte and monocytic series. We observed significant expressions of ACE, renin, and angiotensinogen in K562 leukaemic blast cells. Therefore, K562 human erythroleukaemia cell line may serve as an in vitro model to elucidate the role of RAS in leukaemia and to test the effects of RAS-affecting drugs on leukaemic cellular proliferation.
dc.language.isoen
dc.publisherJ R A A S Ltd
dc.relation.isversionof10.3317/jraas.2007.019
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCardiovascular System & Cardiology
dc.titleRenin-Angiotensin System Expression in the K562 Human Erythroleukaemic Cell Line
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalJournal Of The Renin-Angiotensin-Aldosterone System
dc.contributor.departmentİç Hastalıkları
dc.identifier.volume8
dc.identifier.issue3
dc.identifier.startpage145
dc.identifier.endpage147
dc.description.indexWoS
dc.description.indexScopus


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