Bis induces growth inhibition and differentiation of HL-60 cells via up-regulation of p27

Cited 19 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorY J Seo-
dc.contributor.authorM H Jeon-
dc.contributor.authorJ H Lee-
dc.contributor.authorY J Lee-
dc.contributor.authorH J Youn-
dc.contributor.authorJeong Heon Ko-
dc.contributor.authorJ H Lee-
dc.date.accessioned2017-04-19T09:03:57Z-
dc.date.available2017-04-19T09:03:57Z-
dc.date.issued2005-
dc.identifier.issnI000-0028-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7246-
dc.description.abstractBis (Bag-3, CAIR), a Bcl-2-interacting protein, promotes the anti-apoptotic activity of Bcl-2 and increased levels of Bis have been observed in several disease models. The involvement of Bcl-2 and some Bcl-2-binding proteins in differentiation has recently been reported. However, the relevance of Bis to cellular differentiation remains unknown. The findings herein show that Bis expression is up-regulated during the differentiation of HL-60 cells. To investigate the effect of Bis expression on differentiation, we established Bis-overexpressing HL-60 cells (HL-60-bis). HL-60-bis cells have a low nuclear: cytoplasmic ratio and indented nucleus in Wright-Giemsa staining, and an increased expression of CD11b in immunofluorescence study, indicating the promotion of differentiation. The overexpression of Bis also resulted in a retarded cell growth rate, accompanied by the accumulation of HL-60 cells at the G0/G1 phase of the cell cycle, which was sustained during the differentiation process. Western blot analysis revealed that the expression of p27, a representative inducer of cell cycle arrest at the G1 phase, was increased 2.5-fold in HL-60-bis cells compared to HL-60-neo cells. These results suggest that the Bis induced growth inhibition of HL-60 cells promotes G0/G1 phase arrest via up-regulation of p27, which seems to be a prerequisite for differentiation. Further studies will be required to define the exact roles of Bis on cellular differentiation more precisely.-
dc.publisherSpringer-Nature Pub Group-
dc.titleBis induces growth inhibition and differentiation of HL-60 cells via up-regulation of p27-
dc.title.alternativeBis induces growth inhibition and differentiation of HL-60 cells via up-regulation of p27-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number6-
dc.citation.endPage630-
dc.citation.startPage624-
dc.citation.volume37-
dc.contributor.affiliatedAuthorJeong Heon Ko-
dc.contributor.alternativeName서윤지-
dc.contributor.alternativeName전미희-
dc.contributor.alternativeName이정희-
dc.contributor.alternativeName이용준-
dc.contributor.alternativeName윤호중-
dc.contributor.alternativeName고정헌-
dc.contributor.alternativeName이정화-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 37, no. 6, pp. 624-630-
dc.identifier.doi10.1038/emm.2005.76-
dc.subject.keywordBAG3 protein-
dc.subject.keywordCell differentiation-
dc.subject.keywordCyclin-dependent kinase inhibitor p27-
dc.subject.keywordHL-60 cells-
dc.subject.keywordHuman-
dc.subject.localBAG3 protein-
dc.subject.localcell differentiation-
dc.subject.localCell differentiation-
dc.subject.localCyclin-dependent kinase inhibitor p27-
dc.subject.localHL-60 cells-
dc.subject.localHuman-
dc.subject.localHumans-
dc.subject.localhumans-
dc.subject.localhuman-
dc.description.journalClassY-
Appears in Collections:
Synthetic Biology and Bioengineering Research Institute > Genome Editing Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.