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Yingqun Zhou on Muck Rack

Yingqun Zhou

As seen in: Nature, Dove Medical Press, Gastrointestinal Endoscopy
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Articles

TIAL1 regulates the Hippo pathway through an RNA-binding-independent mechanism

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By Lei Lou, Xiaojie Zhu, Haotian Zhao, Zixin Cai, Pengcheng Wei, Shuchang Peng, Xinyue Hu, Ruohan Sun, Xiaotian Tang, Kai Peng, Yanwen He, Feng Gu, Xiyun Deng, Yingqun Zhou, Junhua Zhou, Yirong Wang, Lei Xue, Xiaowei Guo, Qianlong Dai, Yaxian Zhong
| Nature Verified
Abstract The Hippo pathway is an evolutionarily conserved signaling cascade whose dysregulation is implicated in a wide range of diseases. While many RNA-binding proteins (RBPs) regulate this pathway through canonical functions such as modulating mRNA stability and translation, the potential for RBP-mediated regulation via non-canonical, RNA-binding-independent mechanisms remains poorly defined.
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Endoscopic ultrasound mapping of the gastroepiploic vein in sinistral portal hypertension

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By Jun Li, Yilong Wang, Yingqun Zhou, Junshan Wang, Jiao Feng, Chao Huang, Feng Liu
| Gastrointestinal Endoscopy Verified
Affiliations & Notes 1Department of Gastroenterology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China 2Department of Nursing, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China Article Info Publication History: Received December 25, 2025; Accepted March 26, 2026; Published online April 2, 2026 DOI: 10.1016/j.gie.2026.03.037 External LinkAlso available on ScienceDirect External Link Linked Articles
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SMAD4 Limits PARP1 dependent DNA Repair to Render Pancreatic Cancer Cells Sensitive to Radiotherapy - Cell Death & Disease

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By Yang Wang, Yingqun Zhou, Liwei An
| Nature Verified
Abstract Dysregulation of SMAD4 (i.e. somatic mutation) is strongly associated with poor pancreatic ductal adenocarcinoma (PDAC) prognosis, yet the molecular mechanisms remain underlying this relationship obscure. Previously, we discovered that SMAD4 mutation renders pancreatic cancer resistant to radiotherapy via promotion of autophagy.
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