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| 1 | Astrocytic effect of low molecular weight heparin-superoxide dismutase conjugate in interleukin-6 overexpressing mice following local cerebral ischemia显示文摘BACKGROUND:Studies have shown that low molecular weight heparin-superoxide dismutase conjugate exhibits a remarkable neuroprotective effect. OBJECTIVE:To investigate the effect of low molecular weight heparin-superoxide dismutase conjugate on astrocytes in an interleukin-6(IL-6) overexpressing mice following local cerebral ischemia. DESIGN,TIME AND SETTING:Randomized,cytological,controlled,animal study was performed in the Department of Physiology and Neuroscience,Neurology and Biochemistry and Molecular Biology,Medical University of South Carolina from January 2005 to March 2005. MATERIALS:Nine IL-6 transgenic mice,irrespective of gender,were randomly divided into three groups:sham-operated,model,and treatment,with three mice in each group.With exception of the sham-operated group,right middle cerebral artery occlusion was induced in the mice. Expression of glial fibrillary acidic protein,an astrocyte marker,was determined by immunohistochemistry.Low molecular weight heparin-superoxide dismutase conjugate was purchased from Biochemistry and Biotechnique Institute,Shandong University. METHODS:Two minutes prior to ischemia induction,0.5 mL/kg saline or 20 000 U/kg low molecular weight heparin-superoxide dismutase conjugate were administrated via the femoral artery in the model group and treatment group,respectively.The sham-operated group underwent the same protocols,with the exception of occlusion and treatment. MAIN OUTCOME MEASURES:The number of glial fibrillary acidic protein-positive cells was quantified under light microscopy(x200). RESULTS:In the sham-operated group,there were a large number of astrocytes in the IL-6 transgenic mice.However,the cell bodies were small,and the branches were few and thin.The number of astrocytes in the model group was remarkably less than the sham-operated group. Compared to the model and sham-operated groups,the number of astrocytes significantly increased,and the cell body became larger,following treatment with low molecular weight heparin-superoxide dismutase conjugate.Astrocytes exhibited hypertrophy and hyperplasia,and the processes became longer and thicker. CONCLUSION:The low molecular weight heparin-superoxide dismutase conjugate may provide neuroprotection through astrocytic activation at the super-early stage of cerebral ischemia and reperfusion. | Yizhao Li Guixiang Cui Qingde Wang Hongxia Liu Xiaoxia Zhang Fengshan Wang Keqin Xie | 2009 | Neural Regeneration Research2009，4，2： | 1 |
| 2 | Acrylamide Alters Cytoskeletal Protein Level in Rat Sciatic Nerves显示文摘 | Sufang Yu Fuyong Son Jinxia Yu Xiulan Zhao Lihua Yu Guozhen Li Keqin Xie | 2006 | Neurochemical Research2006，，10： | 1 |
| 3 | Neurofilaments degradation as an early molecular event in tri-ortho-cresyl phosphate (TOCP) induced delayed neuropathy显示文摘 | Fuyong Song Yongjian Yan Xiulan Zhao Cuili Zhang Keqin Xie | 2009 | Toxicology2009，，2： | 1 |
| 4 | Primary structure of Beijing duck apolipoprotein A-1显示文摘 | Zi-Wei Gu Yong-Hong Xie Manlan Yang James T. Sparrow Keqin Wang You Li Wen-Hsiung Li Antonio M. Gotto Chao-Yuh Yang | 1993 | Journal of Protein Chemistry1993，，5： | 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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