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您的检索式：作者名="Chuangpeng Li"
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| 1 | The STX17-SNAP47-VAMP7/VAMP8 complex is the default SNARE complex mediating autophagosome–lysosome fusion显示文摘Autophagosome–lysosome fusion mediated by SNARE complexes is an essential step in autophagy.Two SNAP29-containing SNARE complexes have been extensively studied in starvation-induced bulk autophagy,while the relevant SNARE complexes in other types of autophagy occurring under non-starvation conditions have been overlooked.Here,we found that autophagosome–lysosome fusion in selective autophagy under non-starvation conditions does not require SNAP29-containing SNARE complexes,but requires the STX17-SNAP47-VAMP7/VAMP8 SNARE complex.Further,the STX17-SNAP47-VAMP7/VAMP8 SNARE complex also functions in starvation-induced autophagy.SNAP47 is recruited to autophagosomes following concurrent detection of ATG8s and PI(4,5)P2 via its Pleckstrin homology domain.By contrast,SNAP29-containing SNAREs are excluded from selective autophagy due to inactivation by O-GlcNAcylation under non-starvation conditions.These findings depict a previously unknown,default SNARE complex responsible for autophagosome–lysosome fusion in both selective and bulk autophagy,which could guide research and therapeutic development in autophagy-related diseases. | Fenglei Jian Shen Wang Rui Tian Yufen Wang Chuangpeng Li Yan Li Shixuan Wang Chao Fang Cong Ma Yueguang Rong | 2024 | Cell Research2024，34，2： | 0 |
| 2 | Hepatic Zbtb18 (Zinc Finger and BTB Domain Containing 18) alleviates hepatic steatohepatitis via FXR (Farnesoid X Receptor)显示文摘A lasting imbalance between fatty acid synthesis and consumption leads to non-alcoholic fatty liver disease(NAFLD),coupled with hepatitis and insulin resistance.Yet the details of the underlying mechanisms are not fully understood.Here,we unraveled that the expression of the transcription factor Zbtb18 is markedly decreased in the livers of both patients and murine models of NAFLD.Hepatic Zbtb18 knockout promoted NAFLD features like impaired energy expenditure and fatty acid oxidation(FAO),and induced insulin resistance.Conversely,hepatic Zbtb18 overexpression alleviated hepato-steatosis,insulin resistance,and hyperglycemia in mice fed on a high-fat diet(HFD)or in diabetic mice.Notably,in vitro and in vivo mechanistic studies revealed that Zbtb18 transcriptional activation of Farnesoid X receptor(FXR)mediated FAO and Clathrin Heavy Chain(CLTC)protein hinders NLRP3 inflammasome activity.This key mechanism by which hepatocyte’s Zbtb18 expression alleviates NAFLD and consequent liver fibrosis was further verified by FXR’s deletion and forced expression in mice and cultured mouse primary hepatocytes(MPHs).Moreover,CLTC deletion significantly abrogated the hepatic Zbtb18 overexpression-driven inhibition of NLRP3 inflammasome activity in macrophages.Altogether,Zbtb18 transcriptionally activates the FXR-mediated FAO and CLTC expression,which inhibits NLRP3 inflammasome’s activity alleviating inflammatory stress and insulin resistance,representing an attractive remedy for hepatic steatosis and fibrosis. | Lei Zhang Jiabing Chen Xiaoying Yang Chuangpeng Shen Jiawen Huang Dong Zhang Naihua Liu Chaonan Liu Yadi Zhong Yingjian Chen Kaijia Tang Jingyi Guo Tianqi Cui Siwei Duan Jiayu Li Shangyi Huang Huafeng Pan Huabing Zhang Xiaoqiang Tang Yongsheng Chang Yong Gao | 2024 | Signal Transduction and Targeted Therapy2024，9，2： | 0 |
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