Lifeng Yuan
Duke University
9 Papers
Lifeng Yuan is an academic researcher from Duke University. The author has contributed to research in topics: Biology & Senescence. The author has an hindex of 7, co-authored 8 publications.
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Papers
Cancer-cell-derived GABA promotes β-catenin-mediated tumour growth and immunosuppression
De Huang,Yan Wang,Jill Thompson,Tao Yin,Peter B. Alexander,Di-Yuan Qin,Poorva Mudgal,Haiyang Wu,Yaosi Liang,Lianmei Tan,Christopher C. Pan,Lifeng Yuan,Ying Wan,Qi-Jing Li,Xiao-Fan Wang +14 more
TL;DR: In this article , a cancer cells with aberrant expression of glutamate decarboxylase 1 (GAD1) rewire glutamine metabolism for the synthesis of γ-aminobutyric acid (GABA) in non-nervous tissues.
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MiR-215 Is Induced Post-transcriptionally via HIF-Drosha Complex and Mediates Glioma-Initiating Cell Adaptation to Hypoxia by Targeting KDM1B.
Jing Hu,Tao Sun,Hui Wang,Zhengxin Chen,Shuai Wang,Lifeng Yuan,Tingyu Liu,Hairi Li,Pingping Wang,Yukuan Feng,Qinhong Wang,Roger E. McLendon,Allan H. Friedman,Stephen T. Keir,Darell D. Bigner,Jeffrey C. Rathmell,Xiang-Dong Fu,Qi-Jing Li,Huibo Wang,Xiao-Fan Wang +19 more
TL;DR: It is reported that hypoxia-induced miR-215 is vital for reprograming GICs to fit the hypoxic microenvironment via suppressing the expression of an epigenetic regulator KDM1B and modulating activities of multiple pathways.
106
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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Switching off IMMP2L signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.
Lifeng Yuan,Linhui Zhai,Lili Qian,De Huang,Yi Ding,Handan Xiang,Xiaojing Liu,J. Will Thompson,Juan Liu,Yonghan He,Xiao-Qiong Chen,Jing Hu,Qing-Peng Kong,Minjia Tan,Xiao-Fan Wang +14 more
TL;DR: Mechanistically, it is demonstrated that switching off the specific mitochondrial processing machinery involving the peptidase IMMP2L serves as the foundation of the senescence program, which was also observed during the mammalian aging process.