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首页> 外文期刊>Journal of cellular physiology. >TGFBR2 is a novel substrate and indirect transcription target of deubiquitylase USP9X in granulosa cells
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TGFBR2 is a novel substrate and indirect transcription target of deubiquitylase USP9X in granulosa cells

机译：TGFBR2是一种新型基质和间接的转录的目标deubiquitylase USP9X颗粒细胞

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Abstract The ubiquitin‐specific peptidase 9 X‐linked (USP9X) is one of the highly conserved members belonging to the ubiquitin‐specific proteases (USPs) family, which has been reported to control substrates‐mediated biological functions through deubiquitinating and stabilizing substrates. Here, we have found that TGFBR2, the type II receptor of the transforming growth factor beta (TGF‐β) signaling pathway, is a novel substrate and indirect transcription target of deubiquitylase USP9X in granulosa cells (GCs). Mechanically, USP9X positively influences the expression of TGFBR2 at different levels through two independent ways: (i) directly targets and deubiquitinates TGFBR2, which maintains the protein stability of TGFBR2 through avoiding degradation mediated by ubiquitin‐proteasome system; (ii) indirectly maintains TGFBR2 messenger RNA (mRNA) expression via SMAD4/miR‐143 axis. Specifically, SMAD4, another substrate of USP9X, acts as a transcription factor and suppresses miR‐143 which inhibits the mRNA level of TGFBR2 by directly binding to its 3′‐untranslated region. Functionally, the maintenance of TGFBR2 by USP9X activates the TGF‐β signaling pathway, which further represses GC apoptosis. Our study highlights a functional micro‐regulatory network composed of deubiquitinase (USP9X), small noncoding RNA (miR‐143) and the TGF‐β signaling pathway, which plays a crucial role in the regulation of GC apoptosis and female fertility.
机译：摘要地理泛素肽酶9X量有关(USP9X)是一种高度保守的成员地理属于泛素蛋白酶(USPs)家庭,已报道控制基质介导的生物函数通过deubiquitinating和稳定的基质。TGFBR2, II型受体的改变生长因子β(TGFβ应承担)信号通路一个新颖的衬底和间接转录的目标deubiquitylase USP9X颗粒细胞(GCs)。TGFBR2在不同水平的表达通过两个独立的方式:直接(i)目标和deubiquitinates TGFBR2,保持蛋白质的稳定性TGFBR2通过避免降解由地理泛素蛋白酶体系统;维护TGFBR2信使核糖核酸(mRNA)表达式通过SMAD4 /米尔143轴。另一个基质USP9X,充当转录因子和抑制米尔143直接抑制TGFBR2的mRNA水平绑定到其3 '非翻译区。功能,维护TGFBR2 USP9X激活地理TGFβ信号通路,进一步压制GC细胞凋亡。突出了一个功能性微监管网络由deubiquitinase (USP9X),小非编码RNA (miR量143)和TGFβ信号途径,起了至关重要的作用GC调节细胞凋亡和女性的生育能力。

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