Show simple item record

dc.contributor.authorBulj, Z
dc.contributor.authorDuchi, S
dc.contributor.authorBevilacqua, A
dc.contributor.authorGherardi, A
dc.contributor.authorDozza, B
dc.contributor.authorPiccinini, F
dc.contributor.authorMariani, GA
dc.contributor.authorLucarelli, E
dc.contributor.authorGiannini, S
dc.contributor.authorDonati, D
dc.contributor.authorMarmiroli, S
dc.date.accessioned2020-12-21T01:29:53Z
dc.date.available2020-12-21T01:29:53Z
dc.date.issued2013-01-01
dc.identifier.citationBulj, Z., Duchi, S., Bevilacqua, A., Gherardi, A., Dozza, B., Piccinini, F., Mariani, G. A., Lucarelli, E., Giannini, S., Donati, D. & Marmiroli, S. (2013). Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells. INTERNATIONAL JOURNAL OF ONCOLOGY, 42 (1), pp.118-126. https://doi.org/10.3892/ijo.2012.1700.
dc.identifier.issn1019-6439
dc.identifier.urihttp://hdl.handle.net/11343/256536
dc.description.abstractThis study was designed to investigate the migratory behavior of adult human mesenchymal stem cells (MSC) and the underlying mechanism. Cell migration was assessed by transwell, wound healing and time-lapse in vivo motility assays. Pharmacological inhibitors were used to determine the potential mechanism responsible for cell migration and invasion. The tests that were implemented revealed that MSC were fairly migratory. Protein kinase B (AKT) was strongly activated at the basal level. Through our analyses we demonstrated that pharmacological inactivation of AKT2 but not AKT1 significantly decreased cell migration and invasion. Although preliminary, collectively our results indicate that AKT2 activation plays a critical role in enabling MSC migration.
dc.languageEnglish
dc.publisherSPANDIDOS PUBL LTD
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleProtein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells
dc.typeJournal Article
dc.identifier.doi10.3892/ijo.2012.1700
melbourne.affiliation.departmentSurgery (St Vincent's)
melbourne.source.titleInternational Journal of Oncology
melbourne.source.volume42
melbourne.source.issue1
melbourne.source.pages118-126
dc.rights.licenseCC BY
melbourne.elementsid1223384
melbourne.contributor.authorDuchi, Serena
dc.identifier.eissn1791-2423
melbourne.accessrightsOpen Access


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record