Bo Wang on Muck Rack

Bo Wang

  • Editor in Chief, China Market
As seen in: Amazon Web Services, AIChE Journal, Color Research & Application, Financial Times, Nature, Wiley, Wiley Online Library, British Pharmacological Society, Memory Studies, New Phytologist and
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Articles

CAF-derived PAI-1 serves as an EGFR ligand and fuels KRAS-mutant pancreatic cancer

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By Yu Wang, Chao Liu, Song Gao, Bo Wang, Hongwei Wang, Zijian Shi, Jiayong Li, Xiaofeng Yao, Xiaofan Guo, Jianwei Zheng, Qianqian Zhou, Zhiqiang Chen, Lei Zheng, Qiang Zhang, Jiang Du, Tianxing Zhou, Zhaoyu Zhang, Weijie Song, Lisha Qi, Yalei Wang, Yuh-Pyng Sher, Min Li, Xuan Zhou, Mien-Chie Hung, Yu Ren, Jihui Hao, Shunjin Xia
| Nature Verified
Abstract Epidermal growth factor receptor (EGFR) activation contributes to pancreatic cancer etiology, yet anti-EGFR therapy offers minimal clinical benefits in patients with KRAS mutations. We report that plasminogen activator inhibitor-1 (PAI-1) derived from cancer-associated fibroblasts (CAFs) is selectively elevated in KRAS-mutant tumors and functions as a ligand of EGFR, contributing to resistance to anti-EGFR therapy.
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Design and Evaluation of Conformationally Locked Indole-Carboxylic Acids as Selective THRβ Agonists against MASH Click to copy article link Article link copied!

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By Bo Wang, Yanhao Dong, Hanxiao Zhu
| ACS Publications
Cite Jump to ExpandCollapse ArticleJuly 1, 2026 Design and Evaluation of Conformationally Locked Indole-Carboxylic Acids as Selective THRβ Agonists against MASH Click to copy article linkArticle link copied! Bo Wang Bo Wang School of Pharmaceutical Sciences & Institute of Materia Medica, Shandong First Medical University & Shandong Academy of Medical Sciences, 6699 Qingdao Road, Jinan, Shandong 250117, China Department of Medicinal Chemistry, Key Laboratory of Chemical Biology (Ministry of...
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CD23 sustains NKT17 cell homeostasis via IL-7Rα-mTORC2 signaling

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By Linlin Niu, Bingqian Tan, Jingting Xu, Guangwei Zhang, Bo Wang, Zuochen Du, Di Yang, Xiaoyu Du, Yao Zhao, Chengxi Zhuang
| Nature Verified
Abstract Invariant natural killer T (iNKT) cells serve as a crucial bridge between innate and adaptive immunity, yet the molecular mechanisms that sustain their subset homeostasis remain incompletely defined. Here, we identify CD23 (FcεRII) as a previously unrecognized intrinsic regulator of NKT17 cell homeostasis. CD23 deficiency selectively diminished NKT17 frequency and IL-17 production in the thymus and spleen, while leaving NKT1 and NKT2 subsets largely unaffected.
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