Imperial College London

DrBarbaraMulloy

Faculty of MedicineDepartment of Metabolism, Digestion and Reproduction

Visiting Professor
 
 
 
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Contact

 

b.mulloy Website

 
 
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Location

 

Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gray:2012:10.1007/978-3-642-23056-1_3,
author = {Gray, E and Hogwood, J and Mulloy, B},
doi = {10.1007/978-3-642-23056-1_3},
journal = {Handb Exp Pharmacol},
pages = {43--61},
title = {The anticoagulant and antithrombotic mechanisms of heparin.},
url = {http://dx.doi.org/10.1007/978-3-642-23056-1_3},
year = {2012}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - The molecular basis for the anticoagulant action of heparin lies in its ability to bind to and enhance the inhibitory activity of the plasma protein antithrombin against several serine proteases of the coagulation system, most importantly factors IIa (thrombin), Xa and IXa. Two major mechanisms underlie heparin's potentiation of antithrombin. The conformational changes induced by heparin binding cause both expulsion of the reactive loop and exposure of exosites of the surface of antithrombin, which bind directly to the enzyme target; and a template mechanism exists in which both inhibitor and enzyme bind to the same heparin molecule. The relative importance of these two modes of action varies between enzymes. In addition, heparin can act through other serine protease inhibitors such as heparin co-factor II, protein C inhibitor and tissue factor plasminogen inhibitor. The antithrombotic action of heparin in vivo, though dominated by anticoagulant mechanisms, is more complex, and interactions with other plasma proteins and cells play significant roles in the living vasculature.
AU - Gray,E
AU - Hogwood,J
AU - Mulloy,B
DO - 10.1007/978-3-642-23056-1_3
EP - 61
PY - 2012///
SN - 0171-2004
SP - 43
TI - The anticoagulant and antithrombotic mechanisms of heparin.
T2 - Handb Exp Pharmacol
UR - http://dx.doi.org/10.1007/978-3-642-23056-1_3
UR - https://www.ncbi.nlm.nih.gov/pubmed/22566220
ER -