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{{Seed}}
[[Image:2ed8.png|left|200px]]


<!--
==Solution structure of the second fibronectin type III domain of human Netrin receptor DCC==
The line below this paragraph, containing "STRUCTURE_2ed8", creates the "Structure Box" on the page.
<StructureSection load='2ed8' size='340' side='right'caption='[[2ed8]]' scene=''>
You may change the PDB parameter (which sets the PDB file loaded into the applet)
== Structural highlights ==
or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
<table><tr><td colspan='2'>[[2ed8]] 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=2ED8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ED8 FirstGlance]. <br>
or leave the SCENE parameter empty for the default display.
</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'>[https://proteopedia.org/fgij/fg.htm?mol=2ed8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ed8 OCA], [https://pdbe.org/2ed8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2ed8 RCSB], [https://www.ebi.ac.uk/pdbsum/2ed8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2ed8 ProSAT], [https://www.topsan.org/Proteins/RSGI/2ed8 TOPSAN]</span></td></tr>
{{STRUCTURE_2ed8| PDB=2ed8 |  SCENE= }}
</table>
== Disease ==
[https://www.uniprot.org/uniprot/DCC_HUMAN DCC_HUMAN] Defects in DCC are the cause of mirror movements type 1 (MRMV1) [MIM:[https://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>
== Function ==
[https://www.uniprot.org/uniprot/DCC_HUMAN 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.<ref>PMID:8861902</ref> <ref>PMID:8187090</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/ed/2ed8_consurf.spt"</scriptWhenChecked>
    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
    <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/main_output.php?pdb_ID=2ed8 ConSurf].
<div style="clear:both"></div>


===Solution structure of the second fibronectin type III domain of human Netrin receptor DCC===
==See Also==
 
*[[Netrin receptor|Netrin receptor]]
 
== References ==
==Disease==
<references/>
Known disease associated with this structure: Colorectal cancer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=120470 120470]]
__TOC__
 
</StructureSection>
==About this Structure==
2ED8 is a 1 chain structure of 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].
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Kigawa, T.]]
[[Category: Large Structures]]
[[Category: Koshiba, S.]]
[[Category: Kigawa T]]
[[Category: RSGI, RIKEN Structural Genomics/Proteomics Initiative.]]
[[Category: Koshiba S]]
[[Category: Tochio, N.]]
[[Category: Tochio N]]
[[Category: Tomizawa, T.]]
[[Category: Tomizawa T]]
[[Category: Yokoyama, S.]]
[[Category: Yokoyama S]]
[[Category: Apoptosis]]
[[Category: Colorectal cancer suppressor]]
[[Category: National project on protein structural and functional analyse]]
[[Category: Nppsfa]]
[[Category: Riken structural genomics/proteomics initiative]]
[[Category: Rsgi]]
[[Category: Structural genomic]]
[[Category: Tumor suppressor protein dcc]]
 
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sun Nov 16 11:43:52 2008''

Latest revision as of 21:49, 29 May 2024

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

2ed8 is a 1 chain structure with sequence from Homo sapiens. Full experimental information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:Solution NMR
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT, TOPSAN

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.

See Also

References

  1. ↑ Srour M, Riviere JB, Pham JM, Dube MP, Girard S, Morin S, Dion PA, Asselin G, Rochefort D, Hince P, Diab S, Sharafaddinzadeh N, Chouinard S, Theoret H, Charron F, Rouleau GA. Mutations in DCC cause congenital mirror movements. Science. 2010 Apr 30;328(5978):592. doi: 10.1126/science.1186463. PMID:20431009 doi:10.1126/science.1186463
  2. ↑ Keino-Masu K, Masu M, Hinck L, Leonardo ED, Chan SS, Culotti JG, Tessier-Lavigne M. Deleted in Colorectal Cancer (DCC) encodes a netrin receptor. Cell. 1996 Oct 18;87(2):175-85. PMID:8861902
  3. ↑ Miyake S, Nagai K, Yoshino K, Oto M, Endo M, Yuasa Y. Point mutations and allelic deletion of tumor suppressor gene DCC in human esophageal squamous cell carcinomas and their relation to metastasis. Cancer Res. 1994 Jun 1;54(11):3007-10. PMID:8187090
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