2cui: Difference between revisions
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==Solution structure of the 31st fibronectin type III domain of the human tenascin X== | |||
<StructureSection load='2cui' size='340' side='right' caption='[[2cui]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | |||
== Structural highlights == | |||
==Disease== | <table><tr><td colspan='2'>[[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]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2CUI FirstGlance]. <br> | ||
</td></tr><tr><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">TNXB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr> | |||
<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2cui FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2cui OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2cui RCSB], [http://www.ebi.ac.uk/pdbsum/2cui PDBsum], [http://www.topsan.org/Proteins/RSGI/2cui TOPSAN]</span></td></tr> | |||
<table> | |||
== 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. | [[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 == | |||
==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> | ||
[[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> | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | |||
== | Check<jmol> | ||
[[ | <jmolCheckbox> | ||
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/cu/2cui_consurf.spt"</scriptWhenChecked> | |||
== | <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked> | ||
<references | <text>to colour the structure by Evolutionary Conservation</text> | ||
</jmolCheckbox> | |||
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf]. | |||
<div style="clear:both"></div> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Inoue, M.]] | [[Category: Inoue, M.]] | ||
