2nbv
From Proteopedia
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==Solution structure of the Rpn13 Pru domain engaging the hPLIC2 UBL domain== | ==Solution structure of the Rpn13 Pru domain engaging the hPLIC2 UBL domain== | ||
| - | <StructureSection load='2nbv' size='340' side='right' caption='[[2nbv | + | <StructureSection load='2nbv' size='340' side='right'caption='[[2nbv]]' scene=''> |
== Structural highlights == | == Structural highlights == | ||
| - | <table><tr><td colspan='2'>[[2nbv]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2NBV OCA]. For a <b>guided tour on the structure components</b> use [ | + | <table><tr><td colspan='2'>[[2nbv]] is a 2 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=2NBV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2NBV FirstGlance]. <br> |
| - | </td></tr> | + | </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=2nbv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2nbv OCA], [https://pdbe.org/2nbv PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2nbv RCSB], [https://www.ebi.ac.uk/pdbsum/2nbv PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2nbv ProSAT]</span></td></tr> |
| - | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | |
</table> | </table> | ||
| - | == Disease == | ||
| - | [[http://www.uniprot.org/uniprot/UBQL2_HUMAN UBQL2_HUMAN]] Defects in UBQLN2 are the cause of amyotrophic lateral sclerosis type 15 with or without frontotemporal dementia (ALS15) [MIM:[http://omim.org/entry/300857 300857]]. A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS15 may develop frontotemporal dementia.<ref>PMID:21857683</ref> <ref>PMID:22892309</ref> <ref>PMID:22717235</ref> <ref>PMID:22560112</ref> | ||
== Function == | == Function == | ||
| - | [ | + | [https://www.uniprot.org/uniprot/ADRM1_HUMAN ADRM1_HUMAN] Functions as a proteasomal ubiquitin receptor. Recruits the deubiquitinating enzyme UCHL5 at the 26S proteasome and promotes its activity.<ref>PMID:16990800</ref> <ref>PMID:17139257</ref> <ref>PMID:16815440</ref> <ref>PMID:16906146</ref> <ref>PMID:18497817</ref> |
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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</div> | </div> | ||
<div class="pdbe-citations 2nbv" style="background-color:#fffaf0;"></div> | <div class="pdbe-citations 2nbv" style="background-color:#fffaf0;"></div> | ||
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| + | ==See Also== | ||
| + | *[[3D structures of ubiquitin|3D structures of ubiquitin]] | ||
== References == | == References == | ||
<references/> | <references/> | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
| - | [[Category: | + | [[Category: Homo sapiens]] |
| - | [[Category: | + | [[Category: Large Structures]] |
| - | [[Category: | + | [[Category: Chen X]] |
| + | [[Category: Walters KJ]] | ||
Current revision
Solution structure of the Rpn13 Pru domain engaging the hPLIC2 UBL domain
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