首页> 美国卫生研究院文献>International Journal of Hematology-Oncology and Stem Cell Research >Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC)
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Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC)

机译:河马途径效应物他夫扎林蛋白在维持脐带间充质干细胞(UC-MSC)的干性中的作用

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摘要

Tafazzin (TAZ) protein has been upregulated in various types of human cancers, although the basis for elevation is uncertain, it has been made definite that the effect of mutation in the hippo pathway, particularly when it is switched off, considerably activates tafazzin transcriptionally and thus this results in tissue or tumor overgrowth. Recent perceptions into the activity of tafazzin, have ascribed to it, a role as stem cell factor in mouse mesenchymal and as well as in neural stem cells. Being a downstream molecule in Hippo signalling, phosphorylation or dephosphorylation of tafazzin gene regulates its transcriptional activity and the stemness of mesenchymal stem cells. Commonly, extracellular matrix controls the stem cell fate commitment and perhaps tafazzin controls stemness through altering the extra cellular matrix. Extracellular matrix is generally made up of prime proteoglycans and the fate stabilization of the resulting lineages is surveilled by engineering these glycans. Tafazzin degradation and addition of proteoglycans affect physical attributes of the extracellular matrix that drives cell differentiation into various lineages. Thus, tafazzin along with major glycans present in the extracellular matrix is involved in imparting stemness. However, there are incoherent molecular events, wherein both tafazzin and the extracellular matrix components, together either activate or inhibit differentiation of stem cells. This review discusses about the role of tafazzin oncoprotein as a stemness factor.
机译:尽管升高的基础尚不确定,但塔夫azzin(TAZ)蛋白已在多种人类癌症中被上调,但已明确确定,河马途径中的突变作用(尤其是当其关闭时)会显着激活tafazzin的转录和转录。因此,这导致组织或肿瘤过度生长。最近对tafazzin活性的认识归因于它在小鼠间充质和神经干细胞中作为干细胞因子的作用。 tafazzin基因作为河马信号转导,磷酸化或去磷酸化的下游分子,可调节其转录活性和间充质干细胞的干性。通常,细胞外基质控制着干细胞的命运,而他信则可能通过改变细胞外基质来控制干性。细胞外基质通常由原蛋白聚糖组成,并且通过工程化这些聚糖来监测所得谱系的命运稳定性。他信(Tafazzin)的降解和蛋白聚糖的添加会影响细胞外基质的物理属性,从而驱动细胞分化成各种谱系。因此,他夫嗪与细胞外基质中存在的主要聚糖一起参与赋予干性。然而,存在不连贯的分子事件,其中他夫嗪和细胞外基质成分一起激活或抑制干细胞的分化。这篇评论讨论了他夫嗪癌蛋白作为干性因子的作用。

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