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Ixonnexin from Tick Saliva Promotes Fibrinolysis by Interacting with Plasminogen and Tissue-Type Plasminogen Activator, and Prevents Arterial Thrombosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F18%3A00490992" target="_blank" >RIV/60077344:_____/18:00490992 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.nature.com/articles/s41598-018-22780-1" target="_blank" >https://www.nature.com/articles/s41598-018-22780-1</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s41598-018-22780-1" target="_blank" >10.1038/s41598-018-22780-1</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Ixonnexin from Tick Saliva Promotes Fibrinolysis by Interacting with Plasminogen and Tissue-Type Plasminogen Activator, and Prevents Arterial Thrombosis

  • Original language description

    Tick saliva is a rich source of modulators of vascular biology. We have characterized Ixonnexin, a member of the ´Basic-tail´ family of salivary proteins from the tick Ixodes scapularis. Ixonnexin is a 104 residues (11.8 KDa), non-enzymatic basic protein which contains 3 disulfide bonds and a C-terminal rich in lysine. It is homologous to SALP14, a tick salivary FXa anticoagulant. Ixonnexin was produced by ligation of synthesized fragments (51-104) and (1-50) followed by folding. Ixonnexin, like SALP14, interacts with FXa. Notably, Ixonnexin also modulates fibrinolysis in vitro by a unique salivary mechanism. Accordingly, it accelerates plasminogen activation by tissue-type plasminogen activator (t-PA) with Km 100 nM, however, it does not affect urokinase-mediated fibrinolysis. Additionally, lysine analogue e-aminocaproic acid inhibits Ixonnexin-mediated plasmin generation implying that lysine-binding sites of Kringle domain(s) of plasminogen or t-PA are involved in this process. Moreover, surface plasmon resonance experiments shows that Ixonnexin binds t-PA, and plasminogen (K-D 10 nM), but not urokinase. These results imply that Ixonnexin promotes fibrinolysis by supporting the interaction of plasminogen with t-PA through formation of an enzymatically productive ternary complex. Finally, in vivo experiments demonstrates that Ixonnexin inhibits FeCl3-induced thrombosis in mice. Ixonnexin emerges as novel modulator of fibrinolysis which may also affect parasite-vector-host interactions.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10603 - Genetics and heredity (medical genetics to be 3)

Result continuities

  • Project

    <a href="/en/project/GAP502%2F12%2F2409" target="_blank" >GAP502/12/2409: Investigating the role of tick salivary protease inhibitors at the interface between ticks, pathogens and the vertebrate host</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Scientific Reports

  • ISSN

    2045-2322

  • e-ISSN

  • Volume of the periodical

    8

  • Issue of the periodical within the volume

    19 March

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    12

  • Pages from-to

  • UT code for WoS article

    000427687600003

  • EID of the result in the Scopus database

    2-s2.0-85044236079