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Ying Lai on Muck Rack

Ying Lai

As seen in: Nature, Wiley Online Library, British Pharmacological Society, MDPI, Cell Press, The Journal of Clinical Investigation, Texas Medical Center, The Journal of Immunology, The Journal of Allergy & Clinical Immunology
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Articles

Human Rhinovirus A16 Infection of Mast Cells Promotes T2 and Non-T2 Immune Responses That Are Modulated by the Airway Epithelium

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By Ying Lai, Ryan Murphy, Matthew Liu
| Wiley Online Library Verified
To the Editor, Respiratory viral infection with major serotype human rhinoviruses (RVs) such as RV A16 (RV16) serves as a common trigger for acute asthma exacerbations and can generate a strong type-2 (T2) immune response in the lower airways of some individuals with asthma [1].
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Secreted phospholipase A2 group X regulates peripheral sensitization to allergen

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By JCI Insight, Ryan Murphy, Ying Lai
| The Journal of Clinical Investigation
ResearchImmunologyPulmonology Open Access | 10.1172/jci.insight.196711 JCI Insight. https://doi.org/10.1172/jci.insight.196711. Copyright © 2026, Murphy et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. View PDF Abstract The molecular mechanisms responsible for the “atopic march” of allergic skin disease to allergic airway disease are incompletely understood.
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Molecular mechanism of cholesterol-dependent membrane fusion in SARS-CoV-2 entry - Signal Transduction and Targeted Therapy

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By Wei Li, Mengdan Wu, Shirong Feng, Jiaming Su, Qian Niu, Weijun Lin, Jiaqi Fan, Lele Cui, Kaiyu Li, Zhaoming Su, Guangwen Lu, Ying Lai, Yijuan Xiang
| Nature Verified
Abstract Enveloped virus invasion relies on spike glycoprotein-mediated membrane fusion. Cholesterol that serves crucial roles in modulating protein conformations and membrane properties, plays an essential role in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cell entry. However, the precise regulatory mechanism of cholesterol in SARS-CoV-2 fusion remains unknown.
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