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Cenjing Wang

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Articles

The m 6 A-mediated epi-transcriptomic dysregulation drives synaptic dysfunction in fragile X syndrome

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By Lu Lu, Avijite Kumer Sarkar, Yanchen Liu, Chunlong Ma, Xuyao Chang, George N. Yoshida, Annie Li, Lauren Schmitt, Yu Zhao, Yaping Liu, Xiong Wang, Ling-Qiang Zhu, Dan Liu, Jason Tchieu, Makoto Miyakoshi, Haining Zhu, Christina Gross, Ernest V. Pedapati, Nathan Salomonis, Craig Erickson, Ziyuan Guo, Phyo Han Thwin, Cenjing Wang, Crace Westerkamp, Maag Chelsey, Monzon Stephanie
| Nature Verified
Abstract Fragile X syndrome (FXS), the leading genetic cause of intellectual disability, arises from FMR1 gene silencing and the subsequent loss of the RNA-binding protein FMRP. N6-methyladenosine (m6A) is a prevalent mRNA modification essential for post-transcriptional regulation. FMRP binds and regulates the stability of m6A-containing transcripts. However, how FMRP deficiency impacts transcriptome-wide m6A modifications in FXS remains unknown.
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