8qe8: Difference between revisions

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'''Unreleased structure'''


The entry 8qe8 is ON HOLD  until Paper Publication
==Structure of the non-canonical CTLH E3 substrate receptor WDR26 bound to NMNAT1 substrate==
 
<StructureSection load='8qe8' size='340' side='right'caption='[[8qe8]], [[Resolution|resolution]] 3.80&Aring;' scene=''>
Authors:  
== Structural highlights ==
 
<table><tr><td colspan='2'>[[8qe8]] is a 8 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8QE8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8QE8 FirstGlance]. <br>
Description:  
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.8&#8491;</td></tr>
[[Category: Unreleased Structures]]
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NMN:BETA-NICOTINAMIDE+RIBOSE+MONOPHOSPHATE'>NMN</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></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=8qe8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8qe8 OCA], [https://pdbe.org/8qe8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8qe8 RCSB], [https://www.ebi.ac.uk/pdbsum/8qe8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8qe8 ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/NMNA1_HUMAN NMNA1_HUMAN] Defects in NMNAT1 are the cause of Leber congenital amaurosis 9 (LCA9) [MIM:[https://omim.org/entry/608553 608553]. A severe dystrophy of the retina, typically becoming evident in the first years of life. Visual function is usually poor and often accompanied by nystagmus, sluggish or near-absent pupillary responses, photophobia, high hyperopia and keratoconus.<ref>PMID:22842230</ref> <ref>PMID:22842231</ref> <ref>PMID:22842229</ref> <ref>PMID:22842227</ref>
== Function ==
[https://www.uniprot.org/uniprot/NMNA1_HUMAN NMNA1_HUMAN] Catalyzes the formation of NAD(+) from nicotinamide mononucleotide (NMN) and ATP. Can also use the deamidated form; nicotinic acid mononucleotide (NaMN) as substrate with the same efficiency. Can use triazofurin monophosphate (TrMP) as substrate. Also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD(+). For the pyrophosphorolytic activity, prefers NAD(+) and NAAD as substrates and degrades NADH, nicotinic acid adenine dinucleotide phosphate (NHD) and nicotinamide guanine dinucleotide (NGD) less effectively. Fails to cleave phosphorylated dinucleotides NADP(+), NADPH and NAADP(+). Protects against axonal degeneration following mechanical or toxic insults.<ref>PMID:17402747</ref>
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Chrustowicz J]]
[[Category: Schulman BA]]
[[Category: Sherpa D]]