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Runwei Yang

As seen in: BioRxiv, Cell Press, The Journal of Clinical Investigation, Academic Radiology
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Articles by Runwei Yang

Alternative splicing–triggered mRNA decay informs splice-switching targets for neurodevelopmental disorders

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By Kaining Hu, Runwei Yang, Jiaming Qiu
| The Journal of Clinical Investigation
Abstract Alternative splicing–triggered nonsense-mediated mRNA decay (AS-NMD) critically regulates gene expression, but the extent to which neuronal genes are regulated by AS-NMD remains understudied. Here, we identified over 3,000 developmentally regulated AS-NMD exons in mouse and human brains and validated them in cultured neurons. AS-NMD suppresses synaptic genes during brain development and differentially regulates more than 200 causal genes for neurodevelopmental disorders (NDDs).
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Cell-type-specific splicing of transcription regulators and Ptbp1 by Rbfox1/2/3 in the developing neocortex

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By Xiangbin Ruan, Kaining Hu, Yalan Yang, Runwei Yang
| BioRxiv
Abstract How master splicing regulators crosstalk with each other and to what extent transcription regulators are differentially spliced remain unclear in the developing brain. Here, cell-type-specific RNA-Seq of the developing neocortex uncover that transcription regulators are enriched for differential splicing, altering protein isoforms or inducing nonsense-mediated mRNA decay.
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Imaging and Liquid Biopsy for Distinguishing True Progression From Pseudoprogression in Gliomas, Current Advances and Challenges

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By Kaishu Li, Qihui Zhu, Junyi Yang, Yin Zheng, Siyuan Du, Meihui Song, Qian Peng, Runwei Yang, Yawei Liu, Ling Qi
| Academic Radiology Verified
Gliomas are aggressive brain tumors with a poor prognosis. Assessing treatment response is challenging because magnetic resonance imaging (MRI) may not distinguish true progression (TP) from pseudoprogression (PsP). This review aims to discuss imaging techniques and liquid biopsies used to distinguish TP from PsP.
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Upregulation of SYNGAP1 expression in mice and human neurons by redirecting alternative splicing

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By Runwei Yang, Xinran Feng, Alejandra Arias-Cavieres, Robin Mitchell
| Cell Press Verified
The Ras GTPase-activating protein SYNGAP1 plays a central role in synaptic plasticity, and de novo SYNGAP1 mutations are among the most frequent causes of autism and intellectual disability. How SYNGAP1 is regulated during development and how to treat SYNGAP1-associated haploinsufficiency remain challenging questions. Here, we characterize an alternative 3′ splice site (A3SS) of SYNGAP1 that induces nonsense-mediated mRNA decay (A3SS-NMD) in mouse and human neural development.
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