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首页> 外文期刊>Nucleus >CLIC4 and Schnurri-2: A dynamic duo in TGFβ signaling with broader implications in cellular homeostasis and disease
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CLIC4 and Schnurri-2: A dynamic duo in TGFβ signaling with broader implications in cellular homeostasis and disease

机译：CLIC4和Schnurri-2：TGFβ信号转导中的动态组合，对细胞稳态和疾病具有更广泛的意义

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摘要

CLIC4 is a highly conserved, multifunctional member of the chloride intracellular channel family of proteins. The protein is largely cytoplasmic but translocates to the nucleus upon a variety of stimuli including TGF-β, TNF-α and etoposide. Nuclear resident CLIC4 causes growth arrest, terminal differentiation and apoptosis. Recently, it was discovered that TGF-β causes CLIC4 to associate with Schnurri-2 and together they translocate to the nucleus and dissociate thereafter. The nuclear function of CLIC4 was further illuminated by the discovery that CLIC4 enhances TGF-β signaling by associating with phospho-Smad2 and 3 and preventing their dephosphorylation. Enhanced TGF-β dependent gene expression and growth inhibition are downstream consequences of this activity of CLIC4. In this article, we speculate on other consequences of the CLIC4 relation to TGF-β signaling and the potential for CLIC4 to participate in other cellular functions related to normal homeostasis and disease.
机译：CLIC4是氯化物细胞内通道蛋白家族的高度保守的多功能成员。该蛋白质主要是细胞质的，但在包括TGF-β，TNF-α和依托泊苷在内的各种刺激下易位至细胞核。核常驻CLIC4导致生长停滞，终末分化和凋亡。最近，发现TGF-β引起CLIC4与Schnurri-2缔合，并且它们一起易位至核并此后解离。 CLIC4的发现进一步揭示了CLIC4的核功能，该发现是CLIC4通过与phospho-Smad2和3缔合并防止其去磷酸化来增强TGF-β信号传导。增强的TGF-β依赖性基因表达和生长抑制是CLIC4活性的下游结果。在本文中，我们推测了CLIC4与TGF-β信号传导有关的其他后果，以及CLIC4参与与正常体内稳态和疾病有关的其他细胞功能的潜力。

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