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Inflammasome sensor NLRP1 disease variant M1184V promotes autoproteolysis and DPP9 complex formation by stabilizing the FIIND domain.

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第一作者： Jonas,Moecking

第一单位： Institute of Structural Biology, Medical Faculty, University of Bonn, Bonn, Germany.

作者： Jonas,Moecking ^[1] ; Pawat,Laohamonthonkul ^[2] ; Kubilay,Meşe ^[1] ; Gregor,Hagelueken ^[1] ; Annemarie,Steiner ^[3] ; Cassandra R,Harapas ^[2] ; Jarrod J,Sandow ^[2] ; Jonathan D,Graves ^[4] ; Seth L,Masters ^[2] ; Matthias,Geyer ^[5]

作者单位： Institute of Structural Biology, Medical Faculty, University of Bonn, Bonn, Germany. ^[1] Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia. ^[2] Institute of Structural Biology, Medical Faculty, University of Bonn, Bonn, Germany; Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia. ^[3] IFM Therapeutics, Boston, Massachusetts, USA. ^[4] Institute of Structural Biology, Medical Faculty, University of Bonn, Bonn, Germany. Electronic address: matthias.geyer@uni-bonn.de. ^[5]

关键词 DPP9 NLRP1 Talabostat Val-boroPro asthma inflammasome

医学主题词衔接蛋白质类, 信号转导(Adaptor Proteins, Signal Transducing);凋亡调节蛋白质类(Apoptosis Regulatory Proteins);二肽基肽酶类和三肽基肽酶类(Dipeptidyl-Peptidases and Tripeptidyl-Peptidases);炎性体(Inflammasomes);人类(Humans);自身免疫疾病(Autoimmune Diseases)

DOI 10.1016/j.jbc.2022.102645

PMID 36309085

发布时间 2023-01-11

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