Homo sapiens Protein C

Grace Neuger '24 and Chloe Webb '23


Contents:


I. Introduction



Human activated protein C is serine amidase that participates in amidolytic and anticoagulant activities. As an anticoagulant, protein C helps to prevent dangerous blood clots that often lead to strokes and heart attacks. It does this by regulating blood clot size and downstream propagation of clots by proteolytically inactivating FVIIIa and FVa, both procoagulant cofactors. Protein C also affects fibrinolysis, inflammation, and protection from septic shock. Protein C binds to the membrane of endothelial cells and often interacts with a cofactor protein, protein S, to form a complex that collects within endothelial platelets.

When protein C is activated by the thrombin-thrombomodulin complex and Ca[II], it forms the activated protein C (aPC), allowing protein C to bind to its cofactor, protein S. The protein C-protein S complex is then able to bind to Factors Va and VIIIa. After binding, the complex cleaves these factors, inhibiting their activity in coagulation.


II. General Structure

Activated protein C is made up of two distinct protein chains joined by a . One chain is a formed from three domains, two of which are epidermal growth factor (EGF)-like. The first EGF-like domain is modified, and characterized by a seven residue insert, causing a lateral bulge, and an additional disulfide. The third domain is a glutamic acid (Gla)-domain. The four disulfide bridges present in the first domain involve Cys residues , , , and . These disulfide bridges form three loops, with the first one being larger than normal. Connecting the two EGF domains is a peptide forming an including residues 83-85 of EGF-1 and 91-93 of the connecting peptide. The amino-terminal sequence of the light chain is Ala-Asn-Ser-Phe-Leu-.

The other chain is a consisting of an active site serine residue and has an amino-terminal sequence of Asp-Pro-Glu-Asp-Gln. The heavy chain consists of a catalytic domain, including the protein active site, , and a .


III. Activation by thrombin

Protein C becomes activated by means of various interactions between thrombin, thrombomodulin, endothelial cell protein C receptor (ECPR), and inactive protein C. Thrombin is a molecule that plays a role in coagulation, fibrinolysis, wound healing, chemotaxis of inflammatory cells, mitogenesis, and brain development. In fibrinolysis, thrombin is responsible for converting fibrinogen to fibrin and activating various blood factors. Incubation with alpha thrombin causes the cleavage of a peptide bond between Arg-Leu. in the amino terminal region of the heavy chain. Thrombin binds to thrombomodulin on the endothelial cell membrane, which interacts with ECPR and causes a conformational change, allowing protein C to bind to the receptor. ECPR binds to protein C at its . This then allows the newly activated protein C to form a complex with protein S and go on to regulate fibrinolysis.


IV. Active Site

Protein C has been found to have a structurally open active site, allowing both substrates and inhibitors to easily access it. Although there are not many loops within the active site, there are several surrounding it. The 37, 60, and 97 loops form an almost continuous chain of residues around one side of the active site, creating a depression on its surface. Inside the active site are side chains of that divide the primed area of the active site from the unprimed area. These residues also create a groove within the active site, which allows the substrates to bind.

The differences between the primed and unprimed sections of the active site allow for binding specificity in those areas. In the primed side of the active site, there are multiple deep cavities. One of these cavities is polar, characterized by , while the other cavity is very non-polar, including and . The non-primed region of the active site is notable for the hydrophilic residue Thr and lack of obstruction within its S2 pocket. This allows for protein C to bind to larger residues than other proteolytic proteins.


V. References

Fukudome, K., and Esmon C.T. (1994). Indendification, cloning, and regulation of a nvoel endothelial cell protein C/activated protein C receptor. The Journal of Biological Chemistry 269(42):26486-26491.

Kisiel, W. (1979). Human plasma protein C: isolation, characterization, and mechanism of activation by thrombin Journal of Clinical Investigation 64(3):761-769.

Mather, T., Oganessyan, V., Hof, P., Huber, R., Foundling, S., Esmon., C., Bode, W. (1996). The 2.8 angstrom crystal structure of Gla-domainless activated protein C. The EMBO Journal 15(24):6822-6831.

Narayanan, S. (1999). Multifunctional roles of thrombin. Annals of Clinical and Laboratory Science 29(4):275-280.

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