2cui
From Proteopedia
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==Solution structure of the 31st fibronectin type III domain of the human tenascin X== | ==Solution structure of the 31st fibronectin type III domain of the human tenascin X== | ||
- | <StructureSection load='2cui' size='340' side='right' caption='[[2cui | + | <StructureSection load='2cui' size='340' side='right'caption='[[2cui]]' scene=''> |
== Structural highlights == | == Structural highlights == | ||
- | <table><tr><td colspan='2'>[[2cui]] is a 1 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[2cui]] is a 1 chain structure with sequence from [https://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]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2CUI FirstGlance]. <br> |
- | </td></tr><tr id=' | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr> |
- | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2cui FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2cui OCA], [https://pdbe.org/2cui PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2cui RCSB], [https://www.ebi.ac.uk/pdbsum/2cui PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2cui ProSAT], [https://www.topsan.org/Proteins/RSGI/2cui TOPSAN]</span></td></tr> |
</table> | </table> | ||
== Disease == | == Disease == | ||
- | [ | + | [https://www.uniprot.org/uniprot/TENX_HUMAN TENX_HUMAN] Defects in TNXB are the cause of tenascin-X deficiency (TNXD) [MIM:[https://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 == | == Function == | ||
- | [ | + | [https://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> |
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
- | [[Category: | + | [[Category: Homo sapiens]] |
- | [[Category: Inoue | + | [[Category: Large Structures]] |
- | [[Category: Kigawa | + | [[Category: Inoue M]] |
- | [[Category: Koshiba | + | [[Category: Kigawa T]] |
- | [[Category: Ohnishi | + | [[Category: Koshiba S]] |
- | + | [[Category: Ohnishi S]] | |
- | [[Category: Tochio | + | [[Category: Tochio N]] |
- | [[Category: Yokoyama | + | [[Category: Yokoyama S]] |
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Current revision
Solution structure of the 31st fibronectin type III domain of the human tenascin X
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Categories: Homo sapiens | Large Structures | Inoue M | Kigawa T | Koshiba S | Ohnishi S | Tochio N | Yokoyama S