Regulatory element in fibrin triggers tension-activated transition from catch to slip bonds.

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作者： Rustem I,Litvinov ^[1] ; Olga,Kononova ^[2] ; Artem,Zhmurov ^[3] ; Kenneth A,Marx ^[4] ; Valeri,Barsegov ^[4] ; D,Thirumalai ^[5] ; John W,Weisel ^[3]

作者单位： Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104. ^[1] Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan 420008, Russian Federation. ^[2] Department of Chemistry, University of Massachusetts Lowell, Lowell, MA 01854. ^[3] Laboratory of Computer and Mathematical Modeling of Biological Systems, Moscow Institute of Physics and Technology, Moscow Region 141700, Russian Federation. ^[4] Laboratory of Mathematical Modeling in Medicine, Sechenov University, Moscow 119991, Russian Federation. ^[5] Department of Chemistry, University of Massachusetts Lowell, Lowell, MA 01854; weisel@pennmedicine.upenn.edu valeri_barsegov@uml.edu. ^[6] Department of Chemistry, University of Texas at Austin, Austin, TX 78712. ^[7] Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104; weisel@pennmedicine.upenn.edu valeri_barsegov@uml.edu. ^[8]

关键词 GPU computing catch-slip bond fibrin polymerization fluctuating bottleneck interface remodeling

主题词结合部位(Binding Sites);钙(Calcium);纤维蛋白(Fibrin);人类(Humans);多蛋白复合物(Multiprotein Complexes)

DOI 10.1073/pnas.1802576115

PMID 30087181

发布时间 2019-02-22

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