Sandbox Reserved 350: Difference between revisions
From Proteopedia
Jump to navigationJump to search
No edit summary |
No edit summary |
||
| Line 7: | Line 7: | ||
='''Introduction'''= | ='''Introduction'''= | ||
Coagulation Factor V originally studied in 1987 by William H. Kane, Akitada Ichinose, Frederick S. Hagen and Earl W. Davie, out of University of Washington, Seattle. <ref name="Old">PMID: 2827731 </ref> | Coagulation Factor V originally studied in 1987 by William H. Kane, Akitada Ichinose, Frederick S. Hagen and Earl W. Davie, out of University of Washington, Seattle. <ref name="Old">PMID: 2827731 </ref> | ||
[http://en.wikipedia.org/wiki/Coagulation_cascade Coagulation] is a complex cascade of a biological reaction that takes place after an injury causing bleeding, to prevent bleeding; A step of hemostatsis, which faccilitates the formation of fibrin. | [http://en.wikipedia.org/wiki/Coagulation_cascade Coagulation] is a complex cascade of a biological reaction that takes place after an injury causing bleeding, to prevent bleeding; A step of hemostatsis, which faccilitates the formation of fibrin. There approiaxmetly 30 known factors which play a role in this massive cascade response. A possible explannation for the sheer complexity associated with what is knwon about this cascade is that tight regulation for the formation of blood clots are crutial. | ||
<br /> | <br /> | ||
The role of Human Coagulation Factor V is to act as a cofactor along with Factor X and Prothrombin (Factor II, inactive) to form a [http://en.wikipedia.org/wiki/Prothrombinase Prothrombinase] complex activating Prothrobin to Thrombin (FIIa). Thrombin is then able to activate Firinogen (Factor I) into Fibrin (FIa), which connects platelets bound at the site of injury; formation of a clot. | The role of Human Coagulation Factor V is to act as a cofactor along with Factor X and Prothrombin (Factor II, inactive) to form a [http://en.wikipedia.org/wiki/Prothrombinase Prothrombinase] complex activating Prothrobin to Thrombin (FIIa). Thrombin is then able to activate Firinogen (Factor I) into Fibrin (FIa), which connects platelets bound at the site of injury; formation of a clot. | ||
<br /> | |||
It is vital for controled blood clot formation based on known human diseases/conditions of irregular clotting which are quiet devastating. Two clear aspects of blood clotting involves either under clotting or excessive clotting. The inability to form a clot leads to excessive bleeding from a minor abration known as hemophila. | |||
<br /> | |||
Thrombosis is the second case, where excessive clotting or clotting when no wound is present results in free floating embolisms or thombuses. Floating free in the blood allows the thrombus to lodge itself within the circulatory system, interferring with orgran downstream of the circulating blood. Unusual blood circulation/clotting by a thrombus are causes of heart attacks, strokes and necrosis of tissue. | |||