2cui: Difference between revisions
m Protected "2cui" [edit=sysop:move=sysop] |
No edit summary |
||
| Line 1: | Line 1: | ||
{{STRUCTURE_2cui| PDB=2cui | SCENE= }} | {{STRUCTURE_2cui| PDB=2cui | SCENE= }} | ||
===Solution structure of the 31st fibronectin type III domain of the human tenascin X=== | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/TENX_HUMAN TENX_HUMAN]] Defects in TNXB are the cause of tenascin-X deficiency (TNXD) [MIM:[http://omim.org/entry/606408 606408]]. TNXD leads to an Ehlers-Danlos-like syndrome characterized by hyperextensible skin, hypermobile joints, and tissue fragility. Tenascin-X-deficient patients, however, lack atrophic scars, a major diagnostic criteria for classic Ehlers-Danlos. Delayed wound healing, which is also common in classic EDS, is only present in a subset of patients. | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/TENX_HUMAN TENX_HUMAN]] Appears to mediate interactions between cells and the extracellular matrix. Substrate-adhesion molecule that appears to inhibit cell migration. Accelerates collagen fibril formation. May play a role in supporting the growth of epithelial tumors.<ref>PMID:17033827</ref> | |||
==About this Structure== | ==About this Structure== | ||
[[2cui]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2CUI OCA]. | [[2cui]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2CUI OCA]. | ||
==Reference== | |||
<references group="xtra"/><references/> | |||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Inoue, M.]] | [[Category: Inoue, M.]] | ||
Revision as of 10:35, 24 March 2013
Solution structure of the 31st fibronectin type III domain of the human tenascin X
Disease
[TENX_HUMAN] Defects in TNXB are the cause of tenascin-X deficiency (TNXD) [MIM:606408]. TNXD leads to an Ehlers-Danlos-like syndrome characterized by hyperextensible skin, hypermobile joints, and tissue fragility. Tenascin-X-deficient patients, however, lack atrophic scars, a major diagnostic criteria for classic Ehlers-Danlos. Delayed wound healing, which is also common in classic EDS, is only present in a subset of patients.
Function
[TENX_HUMAN] Appears to mediate interactions between cells and the extracellular matrix. Substrate-adhesion molecule that appears to inhibit cell migration. Accelerates collagen fibril formation. May play a role in supporting the growth of epithelial tumors.[1]
About this Structure
2cui is a 1 chain structure with sequence from Homo sapiens. Full experimental information is available from OCA.
Reference
- ↑ Egging D, van den Berkmortel F, Taylor G, Bristow J, Schalkwijk J. Interactions of human tenascin-X domains with dermal extracellular matrix molecules. Arch Dermatol Res. 2007 Jan;298(8):389-96. Epub 2006 Oct 11. PMID:17033827 doi:10.1007/s00403-006-0706-9
Proteopedia Page Contributors and Editors (what is this?)
- Homo sapiens
- Inoue, M.
- Kigawa, T.
- Koshiba, S.
- Ohnishi, S.
- RSGI, RIKEN Structural Genomics/Proteomics Initiative.
- Tochio, N.
- Yokoyama, S.
- Cell adhesion
- Extracellular matirx
- Fibronectin type iii domain
- National project on protein structural and functional analyse
- Nppsfa
- Riken structural genomics/proteomics initiative
- Rsgi
- Structural genomic
- Tenascin x precursor