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题目:: Pdx1 maintains β cell identity and function by repressing an α cell program.
作者:: Gao(Tao),McKenna(Brian),Li(Changhong),Reichert(Maximilian),Nguyen(James),Singh(Tarjinder),Yang(Chenghua),Pannikar(Archana),Doliba(Nicolai),Zhang(Tingting),Stoffers(Doris A),Edlund(Helena),Matschinsky(Franz),Stein(Roland),Stanger(Ben Z)
状态:: 发布时间2014-02-10 , 更新时间 2016-10-19
期刊:: Cell Metab
摘要:: Pdx1 is a homeobox-containing transcription factor that plays a key role in pancreatic development and adult β cell function. In this study, we traced the fate of adult β cells after Pdx1 deletion. As expected, β-cell-specific removal of Pdx1 resulted in severe hyperglycemia within days. Surprisingly, a large fraction of Pdx1-deleted cells rapidly acquired ultrastructural and physiological features of α cells, indicating that a robust cellular reprogramming had occurred. Reprogrammed cells exhibited a global transcriptional shift that included derepression of the α cell transcription factor MafB, resulting in a transcriptional profile that closely resembled that of α cells. These findings indicate that Pdx1 acts as a master regulator of β cell fate by simultaneously activating genes essential for β cell identity and repressing those associated with α cell identity. We discuss the significance of these findings in the context of the emerging notion that loss of β cell identity contributes to the pathogenesis of type 2 diabetes.
语言:: eng
DOI:

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