作者: Francesca Grespi , Vivien Landré , Alina Molchadsky , Nicola Di Daniele , Luigi Tonino Marsella
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摘要: The tumour suppressor p53 plays an important role in somatic cell reprogramming. While wild-type reduces reprogramming efficiency, mutant exerts a gain of function activity that leads to increased efficiency. Furthermore, induced pluripotent stem cells expressing lose their pluripotency vivo and form malignant tumours when injected mice. It is therefore great interest identify targets (wild type mutant) are responsible for this phenotype during reprogramming, as these could be exploited therapeutic use, is, formation with high but no oncogenic potential. Here we studied the transcriptional changes microRNA series mouse embryonic fibroblasts have undergone transition wild type, knock out or status order microRNAs whose expression dependent on p53. We identified number microRNAs, known functions differentiation carcinogenesis, which was cells. detected several uncharacterised were regulated differentially different backgrounds, suggesting novel pluripotency.