One nuclear target of these MAP kinase signaling pathways is the transcription factor AP-1. MAP kinases regulate AP-1 transcriptional activity by multiple mechanisms. Here we review recent progress towards understanding AP-1 regulation by the ERK, JNK, and p38 MAP kinase signal transduction pathways.

当前的研究揭示了一种新的机制：GAG在改善TNF-α诱导的MMP-1表达中起关键作用，该表达通过HDF中ERK / AP-1信号的失活导致I型胶原变性。 本研究的结果表明，GAGs作为有效的抗衰老剂，可以减少皱纹，具有潜在的应用前景。 已确定GAGs抑制了ERK激活下游转录因子，激活蛋白-1（AP-1； c-fos和c-jun）的磷酸化，导致基质金属蛋白酶-1（MMP-1）水平降低，并且在TNF-α刺激的HDF中金属蛋白酶-1的组织抑制剂的上调。 此外，GAGs减弱了TNF-α诱导的HDFs的凋 …

In this review, we will attempt to unravel the roles of AP-1 in the regulation of anti-tumor immune responses, with a focus on the regulation of immune checkpoints and Tregs, seeking to extract useful insights for more efficacious immunotherapy.

The RAS/RAF/MEK/ERK signaling pathway is activated by mutation in many cancers. Neighboring ETS and AP-1 DNA binding sequences can act as response elements for transcriptional activation by this pathway. ERK phosphorylation of an ETS transcription factor is one mechanism of activating the RAS/ERK ge …

2022年7月27日 · Mechanistically, SMAD4 was directly phosphorylated by extracellular signal–regulated kinase (ERK) at Ser 367 residue following TCR activation. Therefore, our work has offered previously unidentified, important insights into the function of SMAD4 in promoting CD8 + T cell–mediated cytotoxic immune responses.

2010年4月15日 · The expression of oncogenic HRAS can increase AP1 transcriptional activity by activating ERK and JNK, leading to increased expression of Fos proteins and N-terminal phosphorylation of JUN 99.

2022年3月1日 · We find ADAP1 is an inducible factor interacting with the immune signalosome to selectively amplify the ERK–AP-1 axis. Interestingly, ADAP1-mediated ERK–AP-1 activation is dependent on...

2019年6月19日 · Mechanistically, we showed that ARID1A acts as a co-factor at enhancers occupied by AP1 transcription factors acting downstream of the MEK/ERK pathway. Consistently, loss of ARID1A led to a disruption of KRAS/AP1-dependent enhancer activity, accompanied by a downregulation of expression of the associated target genes.

通过采用染色质免疫沉淀和荧光素酶报告基因分析，我们发现 AP-1 直接与 HIF1α 基因启动子相互作用，从而增强其转录。 ERK 抑制剂 U0126 或曲美替尼与 VEGFR 抑制剂阿帕替尼的联合应用，可叠加抑制裸鼠血管生成和HCC1806肿瘤生长。 这些发现为 TNBC 提供了新的治疗策略。 Angiogenesis is well known to play a critical role in breast cancer.

使用互补生化和细胞测定，我们证明 ADAP1 可诱导地与免疫信号体相互作用，直接刺激 KRAS GTP 酶活性，从而通过靶向激活 ERK-AP-1 轴来增强 T 细胞信号传导。 单细胞转录组学分析显示，ADAP1 功能的丧失会在 T 细胞刺激后减弱基因程序，从而抑制潜伏的 HIV-1 再激活。 我们的综合实验方法将 ADAP1 定义为促进 HIV-1 潜伏期逃逸的 T 细胞程序的意外调谐器。 Immune stimulation fuels cell signaling-transcriptional programs inducing biological responses to …