SGK1 increases tumor cell survival, adhesiveness, invasiveness, motility, and epithelial to mesenchymal transition. It stimulates tumor growth by mechanisms such as activation of K + channels and Ca 2+ channels, Na + /H + exchanger, amino acid and glucose transporters, downregulation of Foxo3a and p53, and upregulation of β-catenin and NFκB.

Western blot results revealed that Sgk1 overexpression significantly induced phosphorylation of IKKα, IκBα, and NF-κB, but contrary results were observed in LV-Sgk1 shRNA-transduced cells (Fig...

Here we have identified IκB kinase α (IKKα) as a novel substrate of SGK1 by using biochemical and bioinformatic approaches. SGK1 directly phosphorylates IKKα at Thr-23 and indirectly activates IKKα at Ser-180.

SGK1 increases tumor cell survival, adhesiveness, invasiveness, motility, and epithelial to mesenchymal transition. It stimulates tumor growth by mechanisms such as activation of K + channels and Ca 2+ channels, Na + /H + exchanger, amino acid and glucose transporters, downregulation of Foxo3a and p53, and upregulation of β-catenin and NFκB.

血清和糖皮质激素调节激酶 (SGK) 是丝氨酸/苏氨酸激酶 AGC 家族的成员，由三种亚型组成：SGK1、SGK2 和 SGK3。 SGK1最初被克隆为大鼠乳腺肿瘤细胞中受血清和糖皮质激素转录刺激的基因。 它在某些癌症中上调，而在另一些癌症中下调。 SGK1 增加肿瘤细胞的存活、粘附性、侵袭性、运动性和上皮间质转化。 它通过激活 K+ 通道和 Ca2+ 通道、Na+/H+ 交换器、氨基酸和葡萄糖转运蛋白、下调 Foxo3a 和 p53 以及上调 β-catenin 和 NFκB 等机制刺激肿瘤生长。 …

SGK1, serum and glucocorticoid-regulated kinase 1. The PDK1-SGK1 axis has been characterized as a drug-resistant mechanism of the PI3Kα inhibitor alpelisib in breast cancer, in which mTORC1 is activated via direct phosphorylation and inhibition of TSC2, a negative mTORC1 regulator, by SGK1 (Castel et al., 2016). In HCC1954 and JIMT1 cells ...

2022年5月12日 · SGK1 increases tumor cell survival, adhesiveness, invasiveness, motility, and epithelial to mesenchymal transition. It stimulates tumor growth by mechanisms such as activation of K+ channels and Ca2+ channels, Na+/H+ exchanger, amino acid and glucose transporters, downregulation of Foxo3a and p53, and upregulation of β-catenin and NFκB.

抑制性 kappa B 激酶 beta (IKKβ)，称为 IKK2，是一种关键的调节激酶，通过其 Ser177 和 Ser181 磷酸化来激活 NF-κB，从而促进 kappa B 抑制剂 (IκB) 的磷酸化，触发其泛素化和降解以激活核因子 kappa-B (NF-κB) 级联。 化学抑制IKKβ或其基因敲除已成为阻断NF-κB介导的肿瘤细胞增殖和迁移以及炎症反应的有效方法。 在这篇综述中，我们总结了IKKβ的结构特征和转导机制，以及从自然资源（如倍半萜类、二萜类、三萜类、黄酮类和生物碱类）和化学合成类（如嘧啶类、吡啶类 …

血清/糖皮质激素调节激酶 1 ( sgk1 ) 是丝氨酸/苏氨酸蛋白激酶基因家族的成员，主要受血清和糖皮质激素调节。 sgk1参与肿瘤和纤维化疾病的发展。然而，关于它们在免疫和炎症疾病中的作用的研究相对较少。

2020年7月15日 · Recent evidence has accumulated that SGK1 acts as an essential Akt-independent mediator of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway in cancer. SGK1 is overexpressed in several tumors, including prostate cancer, colorectal carcinoma, glioblastoma, breast cancer, and endometrial cancer.