This old version of Proteopedia is provided for student assignments while the new version is undergoing repairs. Content and edits done in this old version of Proteopedia after March 1, 2026 will eventually be lost when it is retired in about June of 2026.
Apply for new accounts at the new Proteopedia. Your logins will work in both the old and new versions.
1gd5
From Proteopedia
(Difference between revisions)
| Line 1: | Line 1: | ||
==SOLUTION STRUCTURE OF THE PX DOMAIN FROM HUMAN P47PHOX NADPH OXIDASE== | ==SOLUTION STRUCTURE OF THE PX DOMAIN FROM HUMAN P47PHOX NADPH OXIDASE== | ||
| - | <StructureSection load='1gd5' size='340' side='right'caption='[[1gd5 | + | <StructureSection load='1gd5' size='340' side='right'caption='[[1gd5]]' scene=''> |
== Structural highlights == | == Structural highlights == | ||
| - | <table><tr><td colspan='2'>[[1gd5]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/ | + | <table><tr><td colspan='2'>[[1gd5]] 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=1GD5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1GD5 FirstGlance]. <br> |
| - | </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=1gd5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1gd5 OCA], [https://pdbe.org/1gd5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1gd5 RCSB], [https://www.ebi.ac.uk/pdbsum/1gd5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1gd5 ProSAT]</span></td></tr> | + | </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=1gd5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1gd5 OCA], [https://pdbe.org/1gd5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1gd5 RCSB], [https://www.ebi.ac.uk/pdbsum/1gd5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1gd5 ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
| - | + | [https://www.uniprot.org/uniprot/NCF1_HUMAN NCF1_HUMAN] Defects in NCF1 are the cause of chronic granulomatous disease autosomal recessive cytochrome-b-positive type 1 (CGD1) [MIM:[https://omim.org/entry/233700 233700]. Chronic granulomatous disease is a genetically heterogeneous disorder characterized by the inability of neutrophils and phagocytes to kill microbes that they have ingested. Patients suffer from life-threatening bacterial/fungal infections.<ref>PMID:2011585</ref> <ref>PMID:11133775</ref> | |
== Function == | == Function == | ||
| - | + | [https://www.uniprot.org/uniprot/NCF1_HUMAN NCF1_HUMAN] NCF2, NCF1, and a membrane bound cytochrome b558 are required for activation of the latent NADPH oxidase (necessary for superoxide production).<ref>PMID:19801500</ref> | |
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
| Line 36: | Line 37: | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
| - | [[Category: | + | [[Category: Homo sapiens]] |
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
| - | [[Category: Ago | + | [[Category: Ago T]] |
| - | [[Category: Hiroaki | + | [[Category: Hiroaki H]] |
| - | [[Category: Ito | + | [[Category: Ito T]] |
| - | [[Category: Kohda | + | [[Category: Kohda D]] |
| - | [[Category: Sumimoto | + | [[Category: Sumimoto H]] |
| - | + | ||
| - | + | ||
| - | + | ||
| - | + | ||
Current revision
SOLUTION STRUCTURE OF THE PX DOMAIN FROM HUMAN P47PHOX NADPH OXIDASE
| |||||||||||
Categories: Homo sapiens | Large Structures | Ago T | Hiroaki H | Ito T | Kohda D | Sumimoto H

