2ed8: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| (5 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
==Solution structure of the second fibronectin type III domain of human Netrin receptor DCC== | ==Solution structure of the second fibronectin type III domain of human Netrin receptor DCC== | ||
<StructureSection load='2ed8' size='340' side='right' caption='[[2ed8 | <StructureSection load='2ed8' size='340' side='right'caption='[[2ed8]]' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2ed8]] is a 1 chain structure with sequence from [ | <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> | ||
</td></tr><tr><td class="sblockLbl"><b>[[ | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr> | ||
<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | <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> | ||
<table> | </table> | ||
== Disease == | == 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 == | == 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 == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
Check<jmol> | Check<jmol> | ||
<jmolCheckbox> | <jmolCheckbox> | ||
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ed/2ed8_consurf.spt"</scriptWhenChecked> | <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> | <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked> | ||
<text>to colour the structure by Evolutionary Conservation</text> | <text>to colour the structure by Evolutionary Conservation</text> | ||
</jmolCheckbox> | </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/ | </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> | <div style="clear:both"></div> | ||
==See Also== | |||
*[[Netrin receptor|Netrin receptor]] | |||
== References == | == References == | ||
<references/> | <references/> | ||
| Line 25: | Line 29: | ||
</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: | [[Category: Large Structures]] | ||
[[Category: | [[Category: Kigawa T]] | ||
[[Category: | [[Category: Koshiba S]] | ||
[[Category: Tochio | [[Category: Tochio N]] | ||
[[Category: Tomizawa | [[Category: Tomizawa T]] | ||
[[Category: Yokoyama | [[Category: Yokoyama S]] | ||
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
DiseaseDCC_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] FunctionDCC_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 AlsoReferences
|
| ||||||||||||||||