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dc.contributor.authorAthauda arachchi, PM
dc.contributor.authorChandran, S
dc.date.accessioned2023-08-08T10:20:26Z
dc.date.available2023-08-08T10:20:26Z
dc.date.issued2023-07
dc.identifier.urihttp://ir.kdu.ac.lk/handle/345/6515
dc.description.abstractIntroduction: The ability to switch stem cell differentiation fate in-vitro, is a powerful tool that may allow the generation of large numbers of cells that may be required in order to develop biologically engineered tissues and cells required for therapeutic applications such as pharmacological testing of new medications. The transcription factor (“master switch”) Olig2, alone or in conjunction with Nkx2.2, has been implicated as a key cell fate decider for emerging neuro-glial precursors derived from both embryonic stem (ES) cells and from foetal neural stem (FNS) cells. Methods: The in-vitro system of stem cells devoid of exogenous signaling was developed. Stem cells were manipulated by pIRES plasmid vector driven, constitutively expressed Olig-2 or Olig-2/Nkx2.2 transcription factor system introduced into proliferating embryonic or foetal neural stem cells, following a similar embryological temporal p at t e r ni n g s e q ue nc e s e e n i n - v i v o. Findings: Successful stem cell fate modification could be achieved in-vitro using the transcription factor overexpression system. Substantially different cell fates were noted in the presence of Olig-2 alone and in combination with Nkx2.2, with the achievement of premature glial differentiation. Conclusion: This method, therefore, may be useful to generate rare live human cells (such as Oligodendroglia or specialised myocardial cells) in-vitro.en_US
dc.language.isoenen_US
dc.subjectStem cell re-programming,en_US
dc.subjectfate modulation,en_US
dc.subjectTranscription factorsen_US
dc.titleManipulation of stem cell fate in vitro using plasmid-based transcription factor over-expression systemsen_US
dc.typeArticle Full Texten_US
dc.identifier.facultyFGSen_US
dc.identifier.journalKDU Journal of Multidisciplinary Studiesen_US
dc.identifier.issue1en_US
dc.identifier.volume5en_US
dc.identifier.pgnos11-25en_US


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