2ed8: Difference between revisions
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2ed8]] 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=2ED8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ED8 FirstGlance]. <br> | <table><tr><td colspan='2'>[[2ed8]] 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=2ED8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ED8 FirstGlance]. <br> | ||
</td></tr><tr><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">DCC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr> | </td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">DCC ([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=2ed8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ed8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2ed8 RCSB], [http://www.ebi.ac.uk/pdbsum/2ed8 PDBsum], [http://www.topsan.org/Proteins/RSGI/2ed8 TOPSAN]</span></td></tr> | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ed8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ed8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2ed8 RCSB], [http://www.ebi.ac.uk/pdbsum/2ed8 PDBsum], [http://www.topsan.org/Proteins/RSGI/2ed8 TOPSAN]</span></td></tr> | ||
<table> | </table> | ||
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/DCC_HUMAN DCC_HUMAN]] Defects in DCC are the cause of mirror movements type 1 (MRMV1) [MIM:[http://omim.org/entry/157600 157600]]. A disorder characterized by contralateral involuntary movements that mirror voluntary ones. While mirror movements are occasionally found in young children, persistence beyond the age of 10 is abnormal. Mirror movements occur more commonly in the upper extremities.<ref>PMID:20431009</ref> | [[http://www.uniprot.org/uniprot/DCC_HUMAN DCC_HUMAN]] Defects in DCC are the cause of mirror movements type 1 (MRMV1) [MIM:[http://omim.org/entry/157600 157600]]. A disorder characterized by contralateral involuntary movements that mirror voluntary ones. While mirror movements are occasionally found in young children, persistence beyond the age of 10 is abnormal. Mirror movements occur more commonly in the upper extremities.<ref>PMID:20431009</ref> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Kigawa, T | [[Category: Kigawa, T]] | ||
[[Category: Koshiba, S | [[Category: Koshiba, S]] | ||
[[Category: | [[Category: Structural genomic]] | ||
[[Category: Tochio, N | [[Category: Tochio, N]] | ||
[[Category: Tomizawa, T | [[Category: Tomizawa, T]] | ||
[[Category: Yokoyama, S | [[Category: Yokoyama, S]] | ||
[[Category: Apoptosis]] | [[Category: Apoptosis]] | ||
[[Category: Colorectal cancer suppressor]] | [[Category: Colorectal cancer suppressor]] | ||
[[Category: National project on protein structural and functional analyse]] | [[Category: National project on protein structural and functional analyse]] | ||
[[Category: Nppsfa]] | [[Category: Nppsfa]] | ||
[[Category: Rsgi]] | [[Category: Rsgi]] | ||
[[Category: Tumor suppressor protein dcc]] | [[Category: Tumor suppressor protein dcc]] | ||
Revision as of 21:27, 15 January 2015
Solution structure of the second fibronectin type III domain of human Netrin receptor DCCSolution structure of the second fibronectin type III domain of human Netrin receptor DCC
Structural highlights
Disease[DCC_HUMAN] Defects in DCC are the cause of mirror movements type 1 (MRMV1) [MIM:157600]. A disorder characterized by contralateral involuntary movements that mirror voluntary ones. While mirror movements are occasionally found in young children, persistence beyond the age of 10 is abnormal. Mirror movements occur more commonly in the upper extremities.[1] Function[DCC_HUMAN] Receptor for netrin required for axon guidance. Mediates axon attraction of neuronal growth cones in the developing nervous system upon ligand binding. Its association with UNC5 proteins may trigger signaling for axon repulsion. It also acts as a dependence receptor required for apoptosis induction when not associated with netrin ligand. Implicated as a tumor suppressor gene.[2] [3] Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. References
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