Heling Pan
Chinese Academy of Sciences
19 Papers
62 Citations
Heling Pan is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Necroptosis & RIPK1. The author has an hindex of 10, co-authored 19 publications. Previous affiliations of Heling Pan include Harvard University.
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Papers
Small molecule regulators of autophagy identified by an image-based high-throughput screen
Lihong Zhang,Jia Yu,Heling Pan,Ping Hu,Yan Hao,Wenqing Cai,Hong Zhu,Albert D. Yu,Xin Xie,Dawei Ma,Junying Yuan +10 more
TL;DR: The identification of eight compounds that can induce autophagy and promote long-lived protein degradation are identified and the possibility that some of these drugs may be useful for the treatment of Huntington's and other human diseases associated with the accumulation of misfolded proteins is suggested.
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Chaperone-mediated autophagy is involved in the execution of ferroptosis.
Zheming Wu,Yang Geng,Xiaojuan Lu,Yuying Shi,Guowei Wu,Mengmeng Zhang,Bing Shan,Heling Pan,Junying Yuan +8 more
TL;DR: This study identified 2-amino-5-chloro-N,3-dimethylbenzamide (CDDO), a compound known to inhibit heat shock protein 90 (HSP90), as an inhibitor of necroptosis that could also inhibit ferroptosis, and found that HSP90 defined a common regulatory nodal between necroPTosis and ferroPTosis.
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TBK1 Suppresses RIPK1-Driven Apoptosis and Inflammation during Development and in Aging
Daichao Xu,Taijie Jin,Hong Zhu,Hongbo Chen,Dimitry Ofengeim,Chengyu Zou,Lauren Mifflin,Lifeng Pan,Palak Amin,Wanjin Li,Bing Shan,Masanori Gomi Naito,Huyan Meng,Ying Li,Heling Pan,Liviu Aron,Xian Adiconis,Joshua Z. Levin,Bruce A. Yankner,Junying Yuan,Junying Yuan +20 more
TL;DR: It is shown that in Tbk1+/- mice, the reduced myeloid TAK1 expression promotes all the key hallmarks of ALS/FTD, including neuroinflammation, TDP-43 aggregation, axonal degeneration, neuronal loss, and behavior deficits, which are blocked upon inhibition of RIPK1.
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Necroptosis in development and diseases.
TL;DR: RIPK1 inhibition represents a key therapeutic strategy for treatment of diseases where blocking both necroptosis and apoptosis can be beneficial and regulating the activation of RIPK1 by ubiquitination and phosphorylation is critical.
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1
Panfeng Tao,Jinqiao Sun,Zheming Wu,Shihao Wang,Jun Wang,Wanjin Li,Heling Pan,Renkui Bai,Jiahui Zhang,Ying Wang,Pui Y. Lee,Wenjing Ying,Qinhua Zhou,Jia Hou,Wenjie Wang,Bijun Sun,Mi Yang,Danru Liu,Ran Fang,Huan Han,Zhaohui Yang,Xin Huang,Haibo Li,Natalie Deuitch,Yuan Zhang,Dilan Dissanayake,Katrina Haude,Kirsty McWalter,Chelsea Roadhouse,Jennifer MacKenzie,Jennifer MacKenzie,Ronald M. Laxer,Ivona Aksentijevich,Xiaomin Yu,Xiaochuan Wang,Junying Yuan,Qing Zhou,Qing Zhou +37 more
TL;DR: Two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomal-dominant manner are identified andRIPK1 mutations that prevent caspase-8 cleavage sensitize cells to apoptosis, necroptosis and inflammation are identified.
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