This old version of Proteopedia is provided for student assignments while the new version is undergoing repairs. Content and edits done in this old version of Proteopedia after March 1, 2026 will eventually be lost when it is retired in about June of 2026.


Apply for new accounts at the new Proteopedia. Your logins will work in both the old and new versions.


1ggy

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
-
[[Image:1ggy.png|left|200px]]
 
- 
{{STRUCTURE_1ggy| PDB=1ggy | SCENE= }}
{{STRUCTURE_1ggy| PDB=1ggy | SCENE= }}
- 
===HUMAN FACTOR XIII WITH YTTERBIUM BOUND IN THE ION SITE===
===HUMAN FACTOR XIII WITH YTTERBIUM BOUND IN THE ION SITE===
 +
{{ABSTRACT_PUBMED_9988734}}
-
{{ABSTRACT_PUBMED_9988734}}
+
==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>
 +
 
 +
==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==
Line 14: Line 16:
==Reference==
==Reference==
-
<ref group="xtra">PMID:009988734</ref><references group="xtra"/>
+
<ref group="xtra">PMID:009988734</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Protein-glutamine gamma-glutamyltransferase]]
[[Category: Protein-glutamine gamma-glutamyltransferase]]

Revision as of 11:56, 24 March 2013

Template:STRUCTURE 1ggy

Contents

HUMAN FACTOR XIII WITH YTTERBIUM BOUND IN THE ION SITE

Template:ABSTRACT PUBMED 9988734

Disease

[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]

Function

[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

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

See Also

Reference

  • Fox BA, Yee VC, Pedersen LC, Le Trong I, Bishop PD, Stenkamp RE, Teller DC. Identification of the calcium binding site and a novel ytterbium site in blood coagulation factor XIII by x-ray crystallography. J Biol Chem. 1999 Feb 19;274(8):4917-23. PMID:9988734
  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

Proteopedia Page Contributors and Editors (what is this?)

OCA

Personal tools