research data . Dataset . 2016

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Open Access
  • Published: 15 Jan 2016
<div><p>A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the <i>Mycobacterium ulcerans</i> macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as <i>purpura fulimans</i> and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal...
free text keywords: Uncategorised, Buruli Ulcer Lesions, Endothelial Cell Thrombomodulin, control thrombin generation, ability, Mycobacterium ulcerans macrolide exotoxin mycolactone, surface anticoagulant molecules, Sec 61 translocation, protein C anticoagulant pathway, necrosis, TM activates protein C, BU lesions, HDMVEC
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Dataset . 2016
Provider: figshare
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