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Ying Xue on Muck Rack

Ying Xue

As seen in: Color Research & Application, Nature, Wiley, Wiley Online Library, Journal of Automated Methods and Management in Chemistry, Frontiers, MDPI, Taylor & Francis Online, ACS Publications, BMC Genomics and
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Articles

TMEM87A suppresses ferroptosis and increases cancer immunotherapy resistance by maintaining the Golgi apparatus pH homeostasis

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By Jing Li, Yuhan Zhou, Xiong Li, Songlin Yin, Yuan Gao Verified, Haotian Shang, Yongfeng Lai, Liguo Yang, Ying Xue, Xiaoxiao Li, Zhenzhen Chang, JING CHEN, Xiang Cheng, Xiaoyan Zhang, Qian Chu, Fujia Lu, Weimin Wang
| Nature Verified
Abstract Most membrane-bound organelles have been linked to the initiation and execution of ferroptosis. However, the role of the Golgi apparatus and its resident proteins in ferroptosis remain elusive. Here we show that ferroptosis inducer triggers rapid oxidation of Golgi membrane lipids in the early phase of ferroptosis, resulting in disruption of Golgi pH. The Golgi-localized transmembrane protein TMEM87A is identified to mediate ferroptosis resistance through buffering Golgi pH.
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An Integrated Wasserstein GAN–Transformer Deep Learning Framework for Accurate Raman Spectral Identification of Escherichia coli Strains Click to copy article link Article link copied!

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By Ying Xue, Ying Zhang, Bokang Sun
| dx.doi.org
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ELMO2 is a therapeutic vulnerability in mesenchymal-like and drug-resistant non-small cell lung cancer

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By Min Li, Ying Xue, Yuhan Chang, Fan Xu, Feizhen Wu, Jie Hu, Yijun Song, Xufen Yu, Fei Zhou, Caicun Zhou, Xin Cao, Mei Wang, Qihong Huang, Xinjian Tian
| Nature Verified
Abstract Epithelial-mesenchymal transition drives tumor metastasis and therapeutic resistance, yet few treatments have been developed that target this process. Here, we show that ELMO2 represents a specific vulnerability in mesenchymal-like cells. ELMO2 suppression induces excessive autophagy and cell death via FAK activity inhibition. We identify ELMO3 as a functional paralog that compensates for ELMO2 loss, establishing a synthetic lethal interaction.
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