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.
1evu
From Proteopedia
| Line 1: | Line 1: | ||
| - | [[Image:1evu.png|left|200px]] | ||
| - | |||
{{STRUCTURE_1evu| PDB=1evu | SCENE= }} | {{STRUCTURE_1evu| PDB=1evu | SCENE= }} | ||
| - | |||
===HUMAN FACTOR XIII WITH CALCIUM BOUND IN THE ION SITE=== | ===HUMAN FACTOR XIII WITH CALCIUM BOUND IN THE ION SITE=== | ||
| + | ==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 11: | Line 13: | ||
==See Also== | ==See Also== | ||
*[[Factor XIII|Factor XIII]] | *[[Factor XIII|Factor XIII]] | ||
| + | |||
| + | ==Reference== | ||
| + | <references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Protein-glutamine gamma-glutamyltransferase]] | [[Category: Protein-glutamine gamma-glutamyltransferase]] | ||
Revision as of 18:51, 24 March 2013
Contents |
HUMAN FACTOR XIII WITH CALCIUM BOUND IN THE ION SITE
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
1evu is a 2 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.
