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{{STRUCTURE_2edb|  PDB=2edb  |  SCENE=  }}
===Solution structure of the fourth fibronectin type III domain of human Netrin receptor DCC===


==Disease==
==Solution structure of the fourth fibronectin type III domain of human Netrin receptor DCC==
[[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>  
<StructureSection load='2edb' size='340' side='right'caption='[[2edb]]' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[2edb]] 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=2EDB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2EDB FirstGlance]. <br>
</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=2edb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2edb OCA], [https://pdbe.org/2edb PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2edb RCSB], [https://www.ebi.ac.uk/pdbsum/2edb PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2edb ProSAT], [https://www.topsan.org/Proteins/RSGI/2edb TOPSAN]</span></td></tr>
</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/2edb_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=2edb ConSurf].
<div style="clear:both"></div>


==Function==
==See Also==
[[http://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>
*[[Netrin receptor|Netrin receptor]]
 
== References ==
==About this Structure==
<references/>
[[2edb]] 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=2EDB OCA].
__TOC__
 
</StructureSection>
==Reference==
<references group="xtra"/><references/>
[[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: 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]]

Latest revision as of 21:49, 29 May 2024

Solution structure of the fourth fibronectin type III domain of human Netrin receptor DCCSolution structure of the fourth fibronectin type III domain of human Netrin receptor DCC

Structural highlights

2edb 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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