• Fansen Meng, Jeffrey D. Steimle, Elizabeth Straight, Rich G. Li, Yuka Morikawa, Zohaib Iqbal, Bing Xie, Jun Wang, Wyatt G. Paltzer, Yi Zhao, Chang-Ru Tsai, Lin Liu, Maggie Lim, Rita A. Schack, Daniel Ramirez, Katherine Carlson, Vaibhav Deshmukh, Jason M. Karch, Robia G. Pautler, Xiao Li, James F. Martin*. Gene therapy CM-YAPon protects mouse heart from injury. Nat Cardiovasc Res (2025). https://doi.org/10.1038/s44161-025-00744-9 
  • Highlighted by Nature Research Briefing “Reversible Gene Therapy for Cardiac Repair and Protection” (https://doi.org/10.1038/s44161-025-00747-6).   
  • This study establishes a proof of concept for drug-conditional gene therapy in the heart. Transient activation of YAP not only induced shifts in cardiomyocytes cell states but also reprogrammed the surrounding microenvironment, showing that precise temporal control of regenerative factors can provide therapeutic and protective benefits while minimizing adverse effects. More broadly, this strategy offers a versatile platform for modulating regenerative targets beyond YAP, with potential applications in tissue rejuvenation, repair of other organs, and regenerative medicine. 
• Fansen Meng, Jong Hwan Kim, Chang-Ru Tsai, Jun Wang, Yufeng Shi, Vaibhav Deshmukh, Xiao Li, Jeffrey Steimle, Bing Xie, Rich Li, James F. Martin*. SARS-CoV-2 NSP13 interacts with TEAD to suppress Hippo-YAP signaling. eLife, 2025 Sep 23:13:RP100248.  
  • eLife Assessment : This important study elucidates the molecular function of the SARS-CoV-2 helicase NSP13, which inhibits the transcriptional activity of the YAP/TEAD complex in vitro and in vivo. The evidence supporting the authors' claims is compelling, based on cell biological assays and multi-omic studies. This work contributes to the understanding of the new regulatory mechanism of YAP/TEAD after SARS-CoV-2 infection and will be of interest to researchers investigating COVID-19 infection and the Hippo-YAP signaling pathway. 
• Fansen Meng^#, Zhengyang Yu^#, Dan Zhang^#, Shasha Chen^#, Hongxin Guan, Ruyuan Zhou, Qirou Wu, Qian Zhang, Shengduo Liu, Mukesh Kumar Venkat Ramani, Bing Yang, Xiao-Qun Ba, Jing Zhang, Jun Huang, Xueli Bai, Jun Qin, Xin-Hua Feng, Songying Ouyang, Yan Jessie Zhang, Tingbo Liang, Pinglong Xu*. Induced phase separation of mutant NF2 imprisons the cGAS-STING machinery to abrogate antitumor immunity. Molecular Cell, 2021 Aug 24; S1097-2765(21)00624-9. (# Co-first author) 
  • Previewed in Molecular Cell: Interferon induction held captive in tumor cells, Molecular Cell, 2021, 81(20):4109-4110.  
  • Highlighted by Cancer Research as Breaking Insights: Phase separated mutant NF2 promotes immune evasion, Cancer Research, 2021, 81(20):5129.  
  • Missense mutations of the tumor suppressor Neurofibromin 2 (NF2/Merlin) result in sporadic to frequent occurrences of tumorigenesis in multiple organs. However, the underlying pathogenicity of NF2-related tumorigenesis remains mostly unknown. This study reported phase separation mediated quiescence of cGAS-STING signaling by a mutant tumor suppressor and reveals gain-of-function pathogenesis for NF2-related tumors by regulating antitumor immunity.

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