
SOCS3通过JNK和STAT3信号通路调控AKT - 仁和软件
2015年5月18日 · 蛋白激酶B (AKT)是一种丝氨酸/苏氨酸 (Ser/Thr)蛋白激酶,在某些细胞因子的刺激下,能够调控细胞凋亡和细胞增殖信号,与细胞存活、代谢、迁移、侵袭等密切相关。 在乳腺癌中,AKT的表达随着乳腺癌恶性进展逐渐增高,并且与肿瘤的大小相关,研究表明肿瘤体积越大,AKT阳性表达率也越高 [1]。 越来越多的研究结果表明,AKT在多种肿瘤细胞中都存在异常活化现象,如胃癌、肺癌、子宫内膜癌及恶性黑色素癌等,AKT异常活化与肿瘤的发生、发展、治 …
JNK/PI3K/Akt signaling pathway is involved in myocardial …
2016年6月15日 · Recent studies have demonstrated that diabetes impairs the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway, while insulin resistance syndrome has been associated with alterations of this pathway in diabetic rats after ischemia/reperfusion (I/R), and activation of C-jun N-terminal kinase (JNK) i …
PI3K-Akt信号通路详解:通路激活+通路组成+通路串联+通路检 …
PI3K-Akt信号通路是细胞中一个关键的信号传导网络,它可被多种细胞刺激或毒性损伤所激活,并在调控转录、翻译、增殖、生长和存活等基本细胞功能中扮演重要角色。 当生长因子与细胞膜上的 受体酪氨酸激酶 (RTK)或 G蛋白偶联受体 (GPCR)结合时,它们会分别刺激Ia和Ib类PI3K同工酶。 这些被激活的PI3K在细胞膜上催化磷脂酰肌醇,产生第二信使分子—— 磷脂酰肌醇-3,4, 5-三磷酸酯 (PIP3)。 PIP3随后作为关键分子,帮助激活Akt(蛋白激酶B)。 一旦Akt被激活, …
The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal …
The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and c-Jun N-terminal kinase (JNK) pathway are responsible for regulating a variety of cellular processes including cell growth, migration, invasion and apoptosis. These two pathways are essential to the development and progression of tum …
The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal …
One of the essential downstream signaling pathways of Akt is the c-Jun N-terminal kinase (JNK) signaling pathway, which belongs to a subgroup of mitogen-activated protein kinase (MAPK) signaling pathways. The interaction between PI3K/Akt and JNK pathways is complicated due to the dual roles of JNK signaling in apoptosis.
JNK-Dependent Stat3 Phosphorylation Contributes to Akt …
In the present study, we describe a novel signaling axis of the c-Jun NH2 kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) and its involvement in As 3+ -induced Akt activation in human bronchial epithelial cells.
Akt2 Negatively Regulates Assembly of the POSH-MLK-JNK …
2003年11月28日 · We have shown that the SH3-3 domain of POSH acts to dominantly interfere with endogenous POSH, by titrating endogenous Akt2 away from POSH, and that ectopic expression of this dominant interfering protein both increases activation of the JNK signaling pathway and decreases the level of Akt-phosphorylated MLK3.
JNK and STAT3 signaling pathways converge on Akt-mediated ... - PubMed
2013年1月1日 · Ectopic overexpression of miR-21 promoted Akt activation and phosphorylation of EZH2, whereas inhibiting miR-21 by transfecting the cells with anti-miR-21 inhibited Akt activation and EZH2 phosphorylation. Taken together, these results demonstrate a contribution of the JNK, STAT3 and Akt signaling axis to As ( 3+) -induced EZH2 phosphorylation.
JNK antagonizes Akt-mediated survival signals by …
2005年7月11日 · Here, we show that phosphorylation of 14-3-3 by JNK releases the proapoptotic proteins Bad and FOXO3a from 14-3-3 and antagonizes the effects of Akt signaling. As a result of dissociation, Bad is dephosphorylated and translocates to the mitochondria, where it associates with Bcl-2/Bcl-x L .
AKT is indispensable for coordinating Par-4/JNK cross talk in …
2017年5月22日 · In essence, the deceleration in p21 level occurs through ER stress/JNK/Caspase-3 axis via activation/induction of proapoptotic Par-4 and inhibition of AKT. The molecular dynamics studies...