
Xinyue Wang
Articles
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Jan 18, 2025 |
mdpi.com | Hao Luo |Xinyue Wang |Li Zhang
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
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Jan 11, 2025 |
mdpi.com | Xinyue Wang |Tong Ma |Zhiyuan Chen |Yang Liu
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
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Nov 13, 2024 |
nature.com | Xinyue Wang |William J Jowsey |Boatema Ofori-Anyinam |Nicholas West |Jason Yang |Peter C. Fineran | +3 more
AbstractDrug-resistant strains of Mycobacterium tuberculosis are a major global health problem. Resistance to the front-line antibiotic isoniazid is often associated with mutations in the katG-encoded bifunctional catalase-peroxidase. We hypothesise that perturbed KatG activity would generate collateral vulnerabilities in isoniazid-resistant katG mutants, providing potential pathway targets to combat isoniazid resistance.
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Oct 16, 2024 |
mdpi.com | Wenzhe Li |Xinyue Wang |Yanqing Jiang |Shuning Cui
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
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Sep 2, 2024 |
nature.com | Jing Zhou |Xinyue Wang
AbstractAcquired resistance is inevitable in the treatment of non-small cell lung cancer (NSCLC) with osimertinib, and one of the primary mechanisms responsible for this resistance is the epithelial-mesenchymal transition (EMT). We identify upregulation of the proviral integration site for Moloney murine leukemia virus 1 (PIM1) and functional inactivation of glycogen synthase kinase 3β (GSK3β) as drivers of EMT-associated osimertinib resistance.
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