Hippo通路效应蛋白Tafazzin在维持脐带来源的间充质干细胞(UC-MSC)衰老中的作用。

Madhumala Gopinath, Rosa Di Liddo, Francesco Marotta, Ramachandran Murugesan, Antara Banerjee, Sushmitha Sriramulu, Ganesan Jothimani, Vimala Devi Subramaniam, Srinivasan Narasimhan, Swarna Priya K, Xiao-Feng Sun, Surajit Pathak
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引用次数: 0

摘要

Tafazzin(TAZ)蛋白在各种类型的人类癌症中都被上调,尽管上调的基础尚不确定,但已经确定的是,河马通路中的突变效应,特别是当它被关闭时,会在转录上显著激活Tafazzin-,从而导致组织或肿瘤过度生长。最近人们对tafazzin活性的认识将其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Hippo信号传导的下游分子,磷酸化或去磷酸化调节其转录活性和间充质干细胞的干性。通常,细胞外基质控制干细胞的命运承诺,也许tafazzin通过改变细胞外基质来控制干性。细胞外基质通常由主要蛋白聚糖组成,通过工程化这些聚糖来监测由此产生的谱系的命运稳定性。Tafazzin降解和蛋白多糖的添加影响细胞外基质的物理特性,细胞外基质驱动细胞分化为各种谱系。因此,tafazzin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tafazzin和细胞外基质成分一起激活或抑制干细胞的分化。本文综述了tafazzin癌蛋白作为干性因子的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC).

Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC).

Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC).

Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC).

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.

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