Publications
239 results found
de Groot R, Lane DA, Crawley JTB, 2010, The ADAMTS13 metalloprotease domain: roles of subsites in enzyme activity and specificity, BLOOD, Vol: 116, Pages: 3064-3072, ISSN: 0006-4971
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- Citations: 33
Greaves M, Lane DA, 2010, Aspiring for quality and service, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 8, Pages: 1885-1885, ISSN: 1538-7933
McKinnon TA, Goode EC, Birdsey GM, et al., 2010, Specific N-linked glycosylation sites modulate synthesis and secretion of von Willebrand factor, Blood
Andersson HM, Arantes MJ, Crawley JTB, et al., 2010, Activated protein C cofactor function of protein S: a critical role for Asp95 in the EGF1-like domain, BLOOD, Vol: 115, Pages: 4878-4885, ISSN: 0006-4971
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- Citations: 25
Luken BM, Winn LYN, Emsley J, et al., 2010, The importance of vicinal cysteines, C1669 and C1670, for von Willebrand factor A2 domain function, BLOOD, Vol: 115, Pages: 4910-4913, ISSN: 0006-4971
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- Citations: 40
Pos W, Crawley JTB, Fijnheer R, et al., 2010, An autoantibody epitope comprising residues R660, Y661, and Y665 in the ADAMTS13 spacer domain identifies a binding site for the A2 domain of VWF, BLOOD, Vol: 115, Pages: 1640-1649, ISSN: 0006-4971
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- Citations: 99
Greaves M, Lane DA, 2010, Rewards for commitment and success, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 8, Pages: 1-1, ISSN: 1538-7933
Zanardelli S, Chion ACK, Groot E, et al., 2009, A novel binding site for ADAMTS13 constitutively exposed on the surface of globular VWF, BLOOD, Vol: 114, Pages: 2819-2828, ISSN: 0006-4971
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- Citations: 80
de Groot R, Lane DA, Crawley JTB, 2009, ADAMTS13 metalloprotease domain subsites control cleavage site specificity, Publisher: ELSEVIER SCIENCE INC, Pages: 963-963, ISSN: 1538-7933
Luken BM, Winn LYN, Emsley J, et al., 2009, Stabilisation of the VWF A2 domain by introduction of a disulphide bond prevents binding to and cleavage by ADAMTS13, Publisher: ELSEVIER SCIENCE INC, Pages: 346-346, ISSN: 1538-7933
Luken BM, Pos W, Voorberg J, et al., 2009, TTP autoantibodies define a VWF binding site in the ADAMTS13 spacer domain, Publisher: ELSEVIER SCIENCE INC, Pages: 58-58, ISSN: 1538-7933
Zanardelli S, Chion CKW, Lenting PJ, et al., 2009, Globular VWF interaction with C-terminal domains of ADAMTS13 suggests a two site interaction mechanism leading to proteolysis, Publisher: ELSEVIER SCIENCE INC, Pages: 347-347, ISSN: 1538-7933
de Groot R, Ramroop N, Bardhan A, et al., 2009, Identification of a functional exosite in the ADAMTS13 disintegrin-like domain, Publisher: ELSEVIER SCIENCE INC, Pages: 963-963, ISSN: 1538-7933
Andersson HM, Arantes MJ, Crawley JTB, et al., 2009, Activated protein C cofactor function of protein S: a critical role for the EGF1-like domain, Publisher: ELSEVIER SCIENCE INC, Pages: 37-37, ISSN: 1538-7933
de Groot R, Bardhan A, Ramroop N, et al., 2009, Essential role of the disintegrin-like domain in ADAMTS13 function, BLOOD, Vol: 113, Pages: 5609-5616, ISSN: 0006-4971
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- Citations: 63
Gardner MD, Chion C, de Groot R, et al., 2009, A functional calcium-binding site in the metalloprotease domain of ADAMTS13, Blood, Vol: Vol. 113, Pages: 1149-1157
Greaves M, Lane DA, Rosendaal FR, 2009, On the reporting of clinical trials, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 7, Pages: 1-1, ISSN: 1538-7933
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- Citations: 1
de Groot R, Lane DA, 2008, Shear tango: dance of the ADAMTS13/VWF complex, Blood, Vol: 112, Pages: 1548-1549
Crawley JTB, Lane DA, Woodward M, et al., 2008, Evidence that high von Willebrand factor and low ADAMTS-13 levels independently increase the risk of a non-fatal heart attack, Journal of Thrombosis and Haemostasis, Vol: 6, Pages: 583-588, ISSN: 1538-7933
Background: A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS-13) may influence von Willebrand factor (VWF) levels and consequently the risk of myocardial infarction (MI). Moreover, ADAMTS-13 influences hemostatic plug formation in mouse models. We therefore studied their associations in the Glasgow MI Study (GLAMIS). Methods and results: We measured ADAMTS-13 and VWF antigen levels by ELISAs in stored plasma from a case–control study of 466 MI cases and 484 age- and sex-matched controls from the same north Glasgow population. There was no correlation between ADAMTS-13 and VWF levels in cases or controls. ADAMTS-13 levels correlated positively with serum cholesterol and triglycerides and body mass index, and negatively with high-density lipoprotein-cholesterol. VWF levels correlated with age, fibrinogen and C-reactive protein. In multivariable analyses including risk factors, VWF correlated positively with risk of MI, and ADAMTS-13 correlated negatively with risk of MI. These associations were independent of each other. The association of ADAMTS-13 with risk of MI was observed only in multivariable analysis. Conclusions: VWF and ADAMTS-13 levels were not associated in this study, and showed associations with MI risk in opposite directions but of similar strength. The association of ADAMTS-13 with MI is influenced by lipid levels, and consequently requires further investigation.
McKinnon TA, Chion AC, Millington AJ, et al., 2008, N-linked glycosylation of VWF modulates its interaction with ADAMTS13, Blood
Crawley JTB, Lane DA, 2008, The haemostatic role of tissue factor pathway inhibitor, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 28, Pages: 233-242, ISSN: 1079-5642
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- Citations: 104
Camilleri RS, Cohen H, Mackie IJ, et al., 2008, Prevalence of the ADAMTS-13 missense mutation R1060W in late onset adult thrombotic thrombocytopenic purpura., J Thromb Haemost, Vol: 6, Pages: 331-338
BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is most commonly associated with deficiency or inhibition of von Willebrand factor-cleaving protease (ADAMTS-13) activity. ADAMTS-13 mutations and polymorphisms have been reported in childhood congenital TTP, but their significance in adult onset TTP remains unclear. OBJECTIVES: We sought to identify common ADAMTS-13 mutations in adults with late onset TTP and to investigate whether they may predispose acute clinical episodes of the disorder in adulthood. PATIENTS/METHODS/RESULTS: We detected a missense mutation (C3178T) in exon 24 of ADAMTS-13 in 6/53 (11.3%) adult onset TTP patients, but no normal controls (n = 100). Three of the patients had pregnancy-associated TTP; three had chronic relapsing acute idiopathic TTP. C3178T encodes an arginine to tryptophan (R1060W) substitution in the TSP1-7 domain of ADAMTS-13. In vitro expression of mutant and wild-type ADAMTS-13 demonstrated that R1060W caused severe intracellular retention of ADAMTS-13 (<5% secretion) without affecting its metalloprotease activity. One homozygous and five heterozygous patients were identified. No other causative mutations were discovered, yet all six patients had ADAMTS-13 activity levels <5% at presentation (normal: 66-126%). Antibodies/inhibitors to ADAMTS-13 were detected in three/five heterozygous patients, and all six patients had subnormal antigen levels. Six asymptomatic first-degree relatives, including those of two probands with antibodies, were also heterozygous for C3178T; all but one had subnormal ADAMTS-13 activity. CONCLUSION: The high prevalence of R1060W ADAMTS-13 in adult onset TTP, together with its absence in childhood congenital TTP cases reported elsewhere, suggests it may be a factor in the development of late onset TTP.
Camilleri RS, Cohen H, Mackie IJ, et al., 2008, Prevalence of the ADAMTS-13 missense mutation R1060W in late onset adult thrombotic thrombocytopenic purpura, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 6, Pages: 331-338, ISSN: 1538-7933
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- Citations: 69
Crawley JTB, Zanardelli S, Chion CKNK, et al., 2007, The central role of thrombin in hemostasis, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 5, Pages: 95-101, ISSN: 1538-7933
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- Citations: 238
Lam JK, Chion CKNK, Zanardelli S, et al., 2007, Further characterization of ADAMTS-13 inactivation by thrombin, Journal of Thrombosis and Haemostasis, Vol: 5, Pages: 1010-1018, ISSN: 1538-7933
Background: The multimeric size and platelet-tethering function of von Willebrand factor (VWF) are modulated by the plasma metalloprotease, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS-13). In vitro ADAMTS-13 is susceptible to proteolytic inactivation by thrombin. Objectives: In this study, we aimed to characterize the inactivation of ADAMTS-13 by thrombin and to assess its physiological significance. Methods and results: By N-terminal sequencing of cleavage products, and by mutagenesis, we identified the principal thrombin cleavage sites in ADAMTS-13 as R257 and R1176. Using a library of 76 thrombin mutants, we highlighted the functional importance of exosite I on thrombin in the proteolysis of ADAMTS-13. Proteolysis of ADAMTS-13 by thrombin caused an 8-fold reduction in its affinity for VWF that contributed to its loss of VWF-cleaving function. Intriguingly, thrombin-cleaved ADAMTS-13 both bound and proteolyzed a short recombinant VWF A2 domain substrate (VWF115) normally. Following activation of coagulation in normal plasma, endogenous ADAMTS-13, but not added ADAMTS-13, appeared resistant to coagulation-induced fragmentation. An estimation of the Km for ADAMTS-13 proteolysis by thrombin was appreciably higher than the physiological concentration of ADAMTS-13. This was corroborated by the comparatively low affinity of ADAMTS-13 for thrombin (KD 95 nm). Conclusions: Together, our data suggest that ADAMTS-13 is protected from rapid proteolytic inactivation by thrombin in normal plasma. Whether this remains the case under pathological situations involving elevated/sustained generation of thrombin remains unclear.
Villegas-Mendez A, Montes R, Ambrose LR, et al., 2007, Proteolysis of the endothelial cell protein C receptor by neutrophil proteinase 3, Journal of Thrombosis and Haemostasis, Vol: 5, Pages: 980-988, ISSN: 1538-7933
Background: The endothelial cell protein C receptor (EPCR) presents protein C to the thrombin:thrombomodulin complex on the endothelium of large vessels, and enhances the generation of activated protein C (APC) and activation of protease-activated receptor-1. A previous report has demonstrated binding of soluble (s) EPCR to activated neutrophils via surface proteinase 3 (PR3). Methods: We now report further characterization of this interaction. Activated neutrophils and purified PR3 both decrease endothelial cell (EC) surface EPCR, suggestive of its proteolysis. Results: When added to purified recombinant sEPCR, PR3 produced multiple cleavages, with early products including 20 kDa N-terminal and C-terminal (after Lys176) fragments. The binding of active site blocked PR3 to sEPCR was studied by surface plasmon resonance. Estimates of the KD of 18.5–102 nm were obtained with heterogeneous binding, suggestive of more than a single interaction site. Conclusions: This work demonstrates PR3 binding to and proteolysis of EPCR and suggests a mechanism by which anticoagulant and cell protective pathways can be down-regulated during inflammation.
Chion CKNK, Doggen CJM, Crawley JTB, et al., 2007, ADAMTS13 and von Willebrand factor and the risk of myocardial infarction in men, BLOOD, Vol: 109, Pages: 1998-2000, ISSN: 0006-4971
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- Citations: 103
Greaves M, Lane DA, 2007, Testimony and new challenges, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 5, Pages: 448-449, ISSN: 1538-7933
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- Citations: 1
Castaman G, Biguzzi E, Razzari C, et al., 2007, Association of protein S p.Pro667Pro dimorphism with plasma protein S levels in normal individuals and patients with inherited protein S deficiency, THROMBOSIS RESEARCH, Vol: 120, Pages: 421-426, ISSN: 0049-3848
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- Citations: 6
Preston RJS, Ajzner E, Razzari C, et al., 2006, Multifunctional specificity of the protein C/activated protein C Gla domain, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 281, Pages: 28850-28857
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- Citations: 97
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