Rui Chen
Duke University
12 Papers
54 Citations
Rui Chen is an academic researcher from Duke University. The author has contributed to research in topics: Signal transduction & Biology. The author has an hindex of 11, co-authored 12 publications. Previous affiliations of Rui Chen include Wuhan University.
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Papers
LSm14A is a processing body-associated sensor of viral nucleic acids that initiates cellular antiviral response in the early phase of viral infection
Ying Li,Rui Chen,Qian Zhou,Zhi-Sheng Xu,Chao Li,Shuai Wang,Ai-Ping Mao,Xiao-Dong Zhang,Weiwu He,Hong-Bing Shu +9 more
TL;DR: It is found that LSm14A, a member of the LSm family involved in RNA processing in the processing bodies, binds to synthetic or viral RNA and DNA and mediates IRF3 activation and IFN-β induction.
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The E3 ubiquitin ligase MARCH8 negatively regulates IL-1β-induced NF-κB activation by targeting the IL1RAP coreceptor for ubiquitination and degradation.
TL;DR: The E3 ubiquitin ligase membrane-associated RING-CH (MARCH8) is identified as a suppressor of IL-1β–induced NF-κB- and MAPK-activation pathways and suggests that MARCH8-mediated polyubiquitination and degradation of IL1RAP is an important mechanism for negative regulation of IL–1β-induced signaling pathways.
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miR-33a promotes glioma-initiating cell self-renewal via PKA and NOTCH pathways
Hui Wang,Tao Sun,Jing Hu,Rui Zhang,Yanhua Rao,Shuai Wang,Rui Chen,Roger E. McLendon,Allan H. Friedman,Stephen T. Keir,Darell D. Bigner,Qi-Jing Li,Huibo Wang,Xiao-Fan Wang +13 more
TL;DR: A miR-33a-centered signaling network that promotes GIC maintenance and has potential as a therapeutic target for GBM treatment is revealed.
91
CD36 initiates the secretory phenotype during the establishment of cellular senescence
Mengyang Chong,Tao Yin,Rui Chen,Handan Xiang,Lifeng Yuan,Yi Ding,Christopher C. Pan,Zhen Tang,Peter B. Alexander,Qi-Jing Li,Xiao-Fan Wang +10 more
TL;DR: It is discovered that the scavenger receptor CD36 is rapidly upregulated in multiple cell types in response to replicative, oncogenic, and chemical senescent stimuli, and the Aβ–CD36–NF‐κB signaling axis is uncovered as an important regulator of the senescent cell fate via induction of the SASP.
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