1fie: Difference between revisions

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[[Image:1fie.png|left|200px]]
{{STRUCTURE_1fie|  PDB=1fie  |  SCENE=  }}  
{{STRUCTURE_1fie|  PDB=1fie  |  SCENE=  }}  
===RECOMBINANT HUMAN COAGULATION FACTOR XIII===
{{ABSTRACT_PUBMED_7660355}}


===RECOMBINANT HUMAN COAGULATION FACTOR XIII===
==Disease==
[[http://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Defects in F13A1 are the cause of factor XIII subunit A deficiency (FA13AD) [MIM:[http://omim.org/entry/613225 613225]]. FA13AD is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.<ref>PMID:1353995</ref>


{{ABSTRACT_PUBMED_7660355}}
==Function==
[[http://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Factor XIII is activated by thrombin and calcium ion to a transglutaminase that catalyzes the formation of gamma-glutamyl-epsilon-lysine cross-links between fibrin chains, thus stabilizing the fibrin clot. Also cross-link alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin.


==About this Structure==
==About this Structure==
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==Reference==
==Reference==
<ref group="xtra">PMID:007660355</ref><references group="xtra"/>
<ref group="xtra">PMID:007660355</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Protein-glutamine gamma-glutamyltransferase]]
[[Category: Protein-glutamine gamma-glutamyltransferase]]

Revision as of 10:03, 25 March 2013

Template:STRUCTURE 1fie

RECOMBINANT HUMAN COAGULATION FACTOR XIIIRECOMBINANT HUMAN COAGULATION FACTOR XIII

Template:ABSTRACT PUBMED 7660355

DiseaseDisease

[F13A_HUMAN] Defects in F13A1 are the cause of factor XIII subunit A deficiency (FA13AD) [MIM:613225]. FA13AD is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.[1]

FunctionFunction

[F13A_HUMAN] Factor XIII is activated by thrombin and calcium ion to a transglutaminase that catalyzes the formation of gamma-glutamyl-epsilon-lysine cross-links between fibrin chains, thus stabilizing the fibrin clot. Also cross-link alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin.

About this StructureAbout this Structure

1fie is a 2 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

See AlsoSee Also

ReferenceReference

[xtra 1]

  1. Yee VC, Pedersen LC, Bishop PD, Stenkamp RE, Teller DC. Structural evidence that the activation peptide is not released upon thrombin cleavage of factor XIII. Thromb Res. 1995 Jun 1;78(5):389-97. PMID:7660355
  1. Board P, Coggan M, Miloszewski K. Identification of a point mutation in factor XIII A subunit deficiency. Blood. 1992 Aug 15;80(4):937-41. PMID:1353995

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