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本研究针对宫颈癌治疗靶点匮乏的临床难题,揭示了间隙连接蛋白β5(GJB5)通过新型分子机制驱动肿瘤恶性进展的关键作用。研究人员通过多组学分析和功能实验证实,GJB5与Gαi3蛋白互作激活Akt-mTOR信号通路,显著促进宫颈癌细胞增殖、迁移并抑制凋亡。该发现为宫颈癌靶向治疗提供了全新分子靶点,相关成果发表于《Cell Death and Disease》。
BMPER attenuated PI3K/AKT signaling and suppressed BMP4-driven smooth muscle activation in models of PAH. BMPER overexpression mitigated the vascular remodeling that characterizes pulmonary arterial ...
Investigating tirzepatide's role in Alzheimer's reveals its potential to improve brain function and reduce inflammation, ...
A new AI-driven multimodal fusion system accurately predicts survival outcomes in patients with unresectable liver cancer ...
The FDA approved taletrectinib for ROS1-positive NSCLC. The agent shows efficacy for both new and pretreated cases, including ...
These findings implicate a potential tumor-suppressive role for CBS in cells with aberrant PI3K/AKT pathway activation. Consistent with this concept, in human gastric cancer cells with activated ...
The PI3K/AKT/mTOR pathway plays a key role in regulating processes central to cancer progression. PI3K inhibitors have come to play an increasingly important role in the management of relapsed or ...
Upregulation of both the PI3K/AKT/mTOR and RAS/RAF/MAPK pathways activates the ERα-independent pathway in the absence of estrogen though extranuclear ER signaling, thus causing estrogen-regulated gene ...
This work demonstrates that oncogenic activation of the PI3K-AKT-mTOR signaling pathway suppresses ferroptosis via the sterol regulatory element-binding protein-mediated lipogenesis, and that ...
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