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==Solution structure of the fifth fibronectin type III domain of human Netrin receptor DCC==
==Solution structure of the fifth fibronectin type III domain of human Netrin receptor DCC==
<StructureSection load='2edd' size='340' side='right' caption='[[2edd]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
<StructureSection load='2edd' size='340' side='right'caption='[[2edd]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2edd]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2EDD OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2EDD FirstGlance]. <br>
<table><tr><td colspan='2'>[[2edd]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2EDD OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2EDD FirstGlance]. <br>
</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 HUMAN])</td></tr>
</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">DCC ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2edd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2edd OCA], [http://pdbe.org/2edd PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2edd RCSB], [http://www.ebi.ac.uk/pdbsum/2edd PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2edd ProSAT], [http://www.topsan.org/Proteins/RSGI/2edd TOPSAN]</span></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=2edd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2edd OCA], [https://pdbe.org/2edd PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2edd RCSB], [https://www.ebi.ac.uk/pdbsum/2edd PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2edd ProSAT], [https://www.topsan.org/Proteins/RSGI/2edd 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>   
[[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 ==
== Function ==
[[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>   
[[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 ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Human]]
[[Category: Large Structures]]
[[Category: Kigawa, T]]
[[Category: Kigawa, T]]
[[Category: Koshiba, S]]
[[Category: Koshiba, S]]

Revision as of 15:00, 10 February 2021

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

Structural highlights

2edd is a 1 chain structure with sequence from Human. Full experimental information is available from OCA. For a guided tour on the structure components use FirstGlance.
Gene:DCC (HUMAN)
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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