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| 1 | Study on the alteration ofchemical composition and structure parameters of modified montmorill-onite 显示文摘 | LU Xianjun CUI Xueqi SONG Meining | 2003 | Minerals Engineering2003，，16： | 1 |
| 2 | Effects of dietary carbohydrate sources on the growth performance and hepatic carbohydrate metabolic enzyme activities of juvenile cobia(Rachycentron canadum Linnaeus)显示文摘 | Cui Xianjun Zhou Qicun Liang Haiou | 2010 | Aquaculture Research2010，42，1： | 1 |
| 3 | Study on the alteration of chemical composition and structure parameters of modified montmorillonite显示文摘 | Xianjun Lu Xueqi Cui Meining Song | 2003 | Minerals Engineering2003，，16： | 1 |
| 4 | Highly lymphatic metastatic pancreatic cancer cells possess stem cell-likeproperties显示文摘 | Guopei Luo Jiang Long Xiaobo Cui Zhiwen Xiao Zuqiang Liu Si Shi Liang Liu Chen Liu Jin Xu Min Li Xianjun Yu | 2013 | International Journal of Oncology2013，，： | 1 |
| 5 | Translocation of IGF-1R in endoplasmic reticulum enhances SERCA2 activity to trigger Ca_(ER)^(2+)perturbation in hepatocellular carcinoma显示文摘The well-known insulin-like growth factor 1(IGF1)/IGF-1 receptor(IGF-1R)signaling pathway is overexpressed in many tumors,and is thus an attractive target for cancer treatment.However,results have often been disappointing due to crosstalk with other signals.Here,we report that IGF-1R signaling stimulates the growth of hepatocellular carcinoma(HCC)cells through the translocation of IGF-1R into the ER to enhance sarco-endoplasmic reticulum calcium ATPase 2(SERCA2)activity.In response to ligand binding,IGF-1Rβis translocated into the ER byβ-arrestin2(β-arr2).Mass spectrometry analysis identified SERCA2 as a target of ER IGF-1Rβ.SERCA2 activity is heavily dependent on the increase in ER IGF-1Rβlevels.ER IGF-1Rβphosphorylates SERCA2 on Tyr^(990)to enhance its activity.Mutation of SERCA2-Tyr^(990)disrupted the interaction of ER IGF-1Rβwith SERCA2,and therefore ER IGF-1Rβfailed to promote SERCA2 activity.The enhancement of SERCA2 activity triggered Ca_(ER)^(2+)perturbation,leading to an increase in autophagy.Thapsigargin blocked the interaction between SERCA2and ER IGF-1Rβand therefore SERCA2 activity,resulting in inhibition of HCC growth.In conclusion,the translocation of IGF-1R into the ER triggers Ca_(ER)^(2+)perturbation by enhancing SERCA2 activity through phosphorylating Tyr^(990)in HCC. | Yanan Li Keqin Li Ting Pan Qiaobo Xie Yuyao Cheng Xinfeng Wu Rui Xu Xiaohui Liu Li Liu Jiangming Gao Wenmin Yuan Xianjun Qu Shuxiang Cui | 2023 | Acta Pharmaceutica Sinica B2023，13，9： | 0 |
| 6 | Activation of insulin-like growth factor-1 receptor (IGF-1R) promotes growth of colorectal cancer through triggering the MEX3A-mediated degradation of RIG-Ⅰ显示文摘Insulin-like growth factor-1 receptor(IGF-1R) has been made an attractive anticancer target due to its overexpression in cancers.However,targeting it has often produced the disappointing results as the role played by cross talk with numerous downstream signalings.Here,we report a disobliging IGF-1R signaling which promotes growth of cancer through triggering the E3 ubiquitin ligase MEX3A-mediated degradation of RIG-I.The active β-arrestin-2 scaffolds this disobliging signaling to talk with MEX3A.In response to ligands,IGF-1Rβ activated the basal βarr2 into its active state by phosphorylating the interdomain domain on Tyr64 and Tyr250,opening the middle loop(Leu130-Cys141) to the RING domain of MEX3A through the conformational changes of βarr2.The models of βarr2/IGF-1Rβ and βarr2/MEX3A could interpret the mechanism of the activated-IGF-1R in triggering degradation of RIG-I.The assay of the mutants βarr2Y64Aand βarr2Y250Afurther confirmed the role of these two Tyr residues of the interlobe in mediating the talk between IGF-1Rβ and the RING domain of MEX3A.The truncated-βarr2 and the peptide ATQAIRIF,which mimicked the RING domain of MEX3A could prevent the formation of βarr2/IGF-1Rβ and βarr2/MEX3A complexes,thus blocking the IGF-1R-triggered RIG-I degradation.Degradation of RIG-I resulted in the suppression of the IFN-I-associated immune cells in the TME due to the blockade of the RIG-I-MAVS-IFN-I pathway.Poly(I:C) could reverse anti-PD-L1 insensitivity by recovery of RIG-I.In summary,we revealed a disobliging IGF-1R signaling by which IGF-1Rβ promoted cancer growth through triggering the MEX3A-mediated degradation of RIG-I. | Qiaobo Xie Yanyan Chu Wenmin Yuan Yanan Li Keqin Li Xinfeng Wu Xiaohui Liu Rui Xu Shuxiang Cui Xianjun Qu | 2023 | Acta Pharmaceutica Sinica B2023，13，7： | 0 |
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