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A MIF‐Derived Cyclopeptide that Inhibits MIF Binding and Atherogenic Signaling via the Chemokine Receptor CXCR2
ChemBioChem ( IF 3.2 ) Pub Date : 2020-10-30 , DOI: 10.1002/cbic.202000574 Christine Krammer 1 , Christos Kontos 2 , Manfred Dewor 3 , Kathleen Hille 2 , Beatrice Dalla Volta 2 , Omar El Bounkari 1, 3 , Karin Taş 2 , Dzmitry Sinitski 1 , Markus Brandhofer 1 , Remco T A Megens 4, 5 , Christian Weber 4, 5, 6, 7 , Joshua R Schultz 8, 9 , Jürgen Bernhagen 1, 3, 6, 7 , Aphrodite Kapurniotu 2
ChemBioChem ( IF 3.2 ) Pub Date : 2020-10-30 , DOI: 10.1002/cbic.202000574 Christine Krammer 1 , Christos Kontos 2 , Manfred Dewor 3 , Kathleen Hille 2 , Beatrice Dalla Volta 2 , Omar El Bounkari 1, 3 , Karin Taş 2 , Dzmitry Sinitski 1 , Markus Brandhofer 1 , Remco T A Megens 4, 5 , Christian Weber 4, 5, 6, 7 , Joshua R Schultz 8, 9 , Jürgen Bernhagen 1, 3, 6, 7 , Aphrodite Kapurniotu 2
Affiliation
The specific targeting of the interaction between the atypical chemokine MIF and its receptor CXCR2, and its atherosclerosis‐promoting activity in a tailored peptide‐based approach is illustrated. Based on a structure–activity analysis of short N‐like loop‐derived MIF peptides, the cyclic MIF peptide analogue MIF(cyclo10) was identified as a promising candidate that blocks MIF/CXCR2 and counteracts MIF's inflammatory and pro‐atherogenic activity.
中文翻译:
一种 MIF 衍生环肽,可通过趋化因子受体 CXCR2 抑制 MIF 结合和致动脉粥样硬化信号传导
阐明了非典型趋化因子 MIF 与其受体 CXCR2 之间相互作用的特异性靶向,及其在定制的基于肽的方法中的动脉粥样硬化促进活性。基于短 N 样环衍生 MIF 肽的结构-活性分析,环状 MIF 肽类似物 MIF(cyclo10) 被确定为一种有前途的候选药物,可阻断 MIF/CXCR2 并抵消 MIF 的炎症和促动脉粥样硬化活性。
更新日期:2020-10-30
中文翻译:
一种 MIF 衍生环肽,可通过趋化因子受体 CXCR2 抑制 MIF 结合和致动脉粥样硬化信号传导
阐明了非典型趋化因子 MIF 与其受体 CXCR2 之间相互作用的特异性靶向,及其在定制的基于肽的方法中的动脉粥样硬化促进活性。基于短 N 样环衍生 MIF 肽的结构-活性分析,环状 MIF 肽类似物 MIF(cyclo10) 被确定为一种有前途的候选药物,可阻断 MIF/CXCR2 并抵消 MIF 的炎症和促动脉粥样硬化活性。