Factor XII: Difference between revisions

From WikiMD's Wellness Encyclopedia

CSV import
 
CSV import
 
Line 1: Line 1:
'''Factor XII''' (or '''Hageman factor''') is a protein that in humans is encoded by the F12 gene. It is an enzyme of the serine protease (or serin endopeptidase) class. Factor XII is part of the coagulation cascade and activates [[Factor XI]] and prekallikrein in vitro.
== Factor XII ==


== Function ==
[[File:Coagulation full.svg|thumb|right|Diagram of the coagulation cascade, including Factor XII]]


Factor XII is part of the [[coagulation cascade]] and activates Factor XI and prekallikrein in vitro. Factor XII itself is activated to factor XIIa by negatively charged surfaces, such as glass. This is the starting point of the intrinsic pathway. Factor XII can also be used to start coagulation cascades in laboratory studies.
'''Factor XII''', also known as '''Hageman factor''', is a [[serine protease]] enzyme of the [[coagulation cascade]] in the [[blood coagulation]] process. It is a crucial component of the [[intrinsic pathway]] of blood coagulation.


== Clinical significance ==
=== Structure and Function ===
Factor XII is synthesized in the [[liver]] and circulates in the [[blood plasma]] as an inactive zymogen. Upon contact with negatively charged surfaces, such as exposed [[collagen]] or [[kallikrein]], Factor XII is activated to Factor XIIa. This activation is a key step in the initiation of the intrinsic pathway of coagulation.


Deficiencies of Factor XII do not lead to [[hemorrhage]], but excessive amounts can lead to [[thrombosis]]. Deficiencies can be detected by the activated partial thromboplastin time (aPTT) test—a prolonged aPTT suggests a deficiency of one of the factors. Factor XII deficiency is a rare disorder that is inherited in an autosomal recessive manner. This condition is usually discovered when prolonged clotting times are found on preoperative screening tests.  
Factor XIIa then activates [[Factor XI]], which in turn activates [[Factor IX]], leading to the activation of [[Factor X]] and the conversion of [[prothrombin]] to [[thrombin]]. Thrombin then converts [[fibrinogen]] to [[fibrin]], forming a stable blood clot.


== See also ==
=== Clinical Significance ===
* [[Coagulation]]
Deficiency in Factor XII is a rare condition and is usually asymptomatic, as it does not lead to bleeding disorders. However, it can prolong the activated partial thromboplastin time (aPTT) in laboratory tests. Factor XII deficiency is often discovered incidentally during routine coagulation screening.
* [[Factor XI]]
 
* [[Thrombosis]]
Factor XII has also been implicated in the process of [[inflammation]] and [[angiogenesis]], and its role in [[thrombosis]] is an area of active research.
* [[Hemorrhage]]


== References ==
=== History ===
<references />
Factor XII was first discovered in 1955 by Dr. Oscar Ratnoff and Dr. Jane Colopy, who identified it in a patient named John Hageman, after whom the factor is named. Despite its role in the coagulation cascade, individuals with Factor XII deficiency do not typically experience bleeding problems, which led to further investigations into its function.


== External links ==
== Related Pages ==
* [https://www.wikimd.com/wiki/Factor_XII Factor XII] at WikiMD
* [[Coagulation cascade]]
* [[Factor XI]]
* [[Factor IX]]
* [[Thrombin]]
* [[Fibrinogen]]
* [[Intrinsic pathway]]


[[Category:Coagulation system]]
[[Category:Coagulation system]]
[[Category:Enzymes]]
[[Category:Blood]]
{{stub}}

Latest revision as of 11:17, 15 February 2025

Factor XII[edit]

Diagram of the coagulation cascade, including Factor XII

Factor XII, also known as Hageman factor, is a serine protease enzyme of the coagulation cascade in the blood coagulation process. It is a crucial component of the intrinsic pathway of blood coagulation.

Structure and Function[edit]

Factor XII is synthesized in the liver and circulates in the blood plasma as an inactive zymogen. Upon contact with negatively charged surfaces, such as exposed collagen or kallikrein, Factor XII is activated to Factor XIIa. This activation is a key step in the initiation of the intrinsic pathway of coagulation.

Factor XIIa then activates Factor XI, which in turn activates Factor IX, leading to the activation of Factor X and the conversion of prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin, forming a stable blood clot.

Clinical Significance[edit]

Deficiency in Factor XII is a rare condition and is usually asymptomatic, as it does not lead to bleeding disorders. However, it can prolong the activated partial thromboplastin time (aPTT) in laboratory tests. Factor XII deficiency is often discovered incidentally during routine coagulation screening.

Factor XII has also been implicated in the process of inflammation and angiogenesis, and its role in thrombosis is an area of active research.

History[edit]

Factor XII was first discovered in 1955 by Dr. Oscar Ratnoff and Dr. Jane Colopy, who identified it in a patient named John Hageman, after whom the factor is named. Despite its role in the coagulation cascade, individuals with Factor XII deficiency do not typically experience bleeding problems, which led to further investigations into its function.

Related Pages[edit]