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10.18632/oncotarget.11934 http://scihub22266oqcxt.onion/10.18632/oncotarget.11934 C5470962!5470962 !27626700     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27626700 &cmd=llinks): Failed to open stream: HTTP request failed! 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Isoliquiritigenin suppresses human T Lymphocyte activation via covalently binding cysteine 46 of I?B kinase |pdf=|usr=}}{{27626700 }} gab.com Text Isoliquiritigenin suppresses human T Lymphocyte activation via covalently binding cysteine 46 of I B kinase JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626700 #FOAvip The efficacious practice of precision personalized medicine requires a more exact understanding of the molecular mechanisms of drug, hence then it is necessary to identify the binding site of the drugs derived from natural sources. In the study, we investigated the suppressive effect and underlying mechanism of isoliquiritigenin (2',4',4-trihydroxychalcone; ILG), a phyto-flavonoid, on human T lymphocyte activation in vitro and in vivo. The results showed that ILG dose-dependently suppressed human T cell activation via suppressing I?B? phosphorylation and degradation, NF-?B nuclear translocation and IKK? activity. Molecular docking results predicted that cysteine 46 (Cys-46) is probably the binding site of ILG on IKK?, and this prediction has been validated by competition assay and kinase assay. To further verify the binding site of this compound in vivo, IKK?C46A transgenic (IKK?C46A) mice were generated. We found that ILG had a less potent immune-suppressive effect in homozygous IKK?C46A mice than IKK? wild type (IKK? wt) littermates with the delay-type hypersensitivity (DTH), suggesting that ILG cannot significantly suppress the inflammation due to the mutation of Cys-46 in the transgenic mice. Collectively, our findings indicate that the ILG inhibited T cell activation in vivo and in vitro via directly binding to IKK? Cys46. Twit Text FOAVip Isoliquiritigenin suppresses human T Lymphocyte activation via covalently binding cysteine 46 of I B kinase ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626700 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27626700 #FOAvip English Wikipedia <ref>{{Cite pmid|27626700 }}</ref> Isoliquiritigenin suppresses human T Lymphocyte activation via covalently binding cysteine 46 of I?B kinase #MMPMID27626700 Yan F ; Yang F ; Wang R ; Yao XJ ; Bai L ; Zeng X ; Huang J ; Wong VKW ; Lam CWK ; Zhou H ; Su X ; Liu J ; Li T ; Liu L Oncotarget 2017[May]; 8 (21 ): 34223-34235 PMID27626700 show ga The efficacious practice of precision personalized medicine requires a more exact understanding of the molecular mechanisms of drug, hence then it is necessary to identify the binding site of the drugs derived from natural sources. In the study, we investigated the suppressive effect and underlying mechanism of isoliquiritigenin (2',4',4-trihydroxychalcone; ILG), a phyto-flavonoid, on human T lymphocyte activation in vitro and in vivo. The results showed that ILG dose-dependently suppressed human T cell activation via suppressing I?B? phosphorylation and degradation, NF-?B nuclear translocation and IKK? activity. Molecular docking results predicted that cysteine 46 (Cys-46) is probably the binding site of ILG on IKK?, and this prediction has been validated by competition assay and kinase assay. To further verify the binding site of this compound in vivo, IKK?C46A transgenic (IKK?C46A) mice were generated. We found that ILG had a less potent immune-suppressive effect in homozygous IKK?C46A mice than IKK? wild type (IKK? wt) littermates with the delay-type hypersensitivity (DTH), suggesting that ILG cannot significantly suppress the inflammation due to the mutation of Cys-46 in the transgenic mice. Collectively, our findings indicate that the ILG inhibited T cell activation in vivo and in vitro via directly binding to IKK? Cys46. |Animals [MESH] |Binding Sites/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Chalcones/*administration & dosage/pharmacology [MESH] |Cysteine/*metabolism [MESH] |Dose-Response Relationship, Drug [MESH] |Enzyme Inhibitors/*administration & dosage/pharmacology [MESH] |HEK293 Cells [MESH] |Humans [MESH] |I-kappa B Kinase/*chemistry/genetics/*metabolism [MESH] |Lymphocyte Activation/drug effects [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Models, Molecular [MESH] |Molecular Docking Simulation [MESH] |Phosphorylation/drug effects [MESH] |Protein Binding/drug effects [MESH] |Proteolysis [MESH]Isoliquiritigenin suppresses human T Lymphocyte activation via covalen(epmc).pdf DeepDyve Pubget Overpricing