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==Solution structure of apoWLN5-6==
==Solution structure of apoWLN5-6==
<StructureSection load='2ew9' size='340' side='right' caption='[[2ew9]], [[NMR_Ensembles_of_Models | 31 NMR models]]' scene=''>
<StructureSection load='2ew9' size='340' side='right'caption='[[2ew9]], [[NMR_Ensembles_of_Models | 31 NMR models]]' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2ew9]] 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=2EW9 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2EW9 FirstGlance]. <br>
<table><tr><td colspan='2'>[[2ew9]] 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=2EW9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2EW9 FirstGlance]. <br>
</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">ATP7B, PWD, WC1, WND ([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">ATP7B, PWD, WC1, WND ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Copper-exporting_ATPase Copper-exporting ATPase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.4 3.6.3.4] </span></td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Copper-exporting_ATPase Copper-exporting ATPase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.4 3.6.3.4] </span></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=2ew9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ew9 OCA], [http://pdbe.org/2ew9 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2ew9 RCSB], [http://www.ebi.ac.uk/pdbsum/2ew9 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2ew9 ProSAT]</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=2ew9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ew9 OCA], [https://pdbe.org/2ew9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2ew9 RCSB], [https://www.ebi.ac.uk/pdbsum/2ew9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2ew9 ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/ATP7B_HUMAN ATP7B_HUMAN]] Defects in ATP7B are the cause of Wilson disease (WD) [MIM:[http://omim.org/entry/277900 277900]]. WD is an autosomal recessive disorder of copper metabolism in which copper cannot be incorporated into ceruloplasmin in liver, and cannot be excreted from the liver into the bile. Copper accumulates in the liver and subsequently in the brain and kidney. The disease is characterized by neurologic manifestations and signs of cirrhosis.<ref>PMID:8298641</ref> <ref>PMID:7626145</ref> <ref>PMID:8533760</ref> <ref>PMID:8938442</ref> <ref>PMID:8931691</ref> <ref>PMID:8782057</ref> <ref>PMID:9311736</ref> <ref>PMID:9772425</ref> <ref>PMID:9222767</ref> <ref>PMID:8980283</ref> <ref>PMID:9887381</ref> <ref>PMID:9482578</ref> <ref>PMID:9554743</ref> <ref>PMID:9452121</ref> <ref>PMID:9671269</ref> <ref>PMID:9829905</ref> <ref>PMID:10194254</ref> <ref>PMID:10447265</ref> <ref>PMID:10502776</ref> <ref>PMID:10502777</ref> <ref>PMID:10051024</ref> <ref>PMID:10544227</ref> <ref>PMID:10453196</ref> <ref>PMID:11216666</ref> <ref>PMID:11093740</ref> <ref>PMID:10790207</ref> <ref>PMID:10721669</ref> <ref>PMID:11043508</ref> <ref>PMID:11180609</ref> <ref>PMID:11690702</ref> <ref>PMID:11243728</ref> <ref>PMID:11954751</ref> <ref>PMID:12544487</ref> <ref>PMID:12325021</ref> <ref>PMID:12376745</ref> <ref>PMID:14986826</ref> <ref>PMID:14639035</ref> <ref>PMID:15024742</ref> <ref>PMID:15557537</ref> <ref>PMID:14966923</ref> <ref>PMID:15845031</ref> <ref>PMID:15811015</ref> <ref>PMID:15952988</ref> <ref>PMID:16207219</ref> <ref>PMID:16283883</ref> <ref>PMID:16088907</ref> <ref>PMID:15967699</ref> <ref>PMID:17718866</ref> <ref>PMID:18373411</ref> <ref>PMID:18203200</ref> <ref>PMID:21682854</ref>   
[[https://www.uniprot.org/uniprot/ATP7B_HUMAN ATP7B_HUMAN]] Defects in ATP7B are the cause of Wilson disease (WD) [MIM:[https://omim.org/entry/277900 277900]]. WD is an autosomal recessive disorder of copper metabolism in which copper cannot be incorporated into ceruloplasmin in liver, and cannot be excreted from the liver into the bile. Copper accumulates in the liver and subsequently in the brain and kidney. The disease is characterized by neurologic manifestations and signs of cirrhosis.<ref>PMID:8298641</ref> <ref>PMID:7626145</ref> <ref>PMID:8533760</ref> <ref>PMID:8938442</ref> <ref>PMID:8931691</ref> <ref>PMID:8782057</ref> <ref>PMID:9311736</ref> <ref>PMID:9772425</ref> <ref>PMID:9222767</ref> <ref>PMID:8980283</ref> <ref>PMID:9887381</ref> <ref>PMID:9482578</ref> <ref>PMID:9554743</ref> <ref>PMID:9452121</ref> <ref>PMID:9671269</ref> <ref>PMID:9829905</ref> <ref>PMID:10194254</ref> <ref>PMID:10447265</ref> <ref>PMID:10502776</ref> <ref>PMID:10502777</ref> <ref>PMID:10051024</ref> <ref>PMID:10544227</ref> <ref>PMID:10453196</ref> <ref>PMID:11216666</ref> <ref>PMID:11093740</ref> <ref>PMID:10790207</ref> <ref>PMID:10721669</ref> <ref>PMID:11043508</ref> <ref>PMID:11180609</ref> <ref>PMID:11690702</ref> <ref>PMID:11243728</ref> <ref>PMID:11954751</ref> <ref>PMID:12544487</ref> <ref>PMID:12325021</ref> <ref>PMID:12376745</ref> <ref>PMID:14986826</ref> <ref>PMID:14639035</ref> <ref>PMID:15024742</ref> <ref>PMID:15557537</ref> <ref>PMID:14966923</ref> <ref>PMID:15845031</ref> <ref>PMID:15811015</ref> <ref>PMID:15952988</ref> <ref>PMID:16207219</ref> <ref>PMID:16283883</ref> <ref>PMID:16088907</ref> <ref>PMID:15967699</ref> <ref>PMID:17718866</ref> <ref>PMID:18373411</ref> <ref>PMID:18203200</ref> <ref>PMID:21682854</ref>   
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/ATP7B_HUMAN ATP7B_HUMAN]] Involved in the export of copper out of the cells, such as the efflux of hepatic copper into the bile.  
[[https://www.uniprot.org/uniprot/ATP7B_HUMAN ATP7B_HUMAN]] Involved in the export of copper out of the cells, such as the efflux of hepatic copper into the bile.  
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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==See Also==
==See Also==
*[[ATPase|ATPase]]
*[[ATPase 3D structures|ATPase 3D structures]]
== References ==
== References ==
<references/>
<references/>
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[[Category: Copper-exporting ATPase]]
[[Category: Copper-exporting ATPase]]
[[Category: Human]]
[[Category: Human]]
[[Category: Large Structures]]
[[Category: Ciofi-Baffoni, S]]
[[Category: Ciofi-Baffoni, S]]
[[Category: SPINE, Structural Proteomics in Europe]]
[[Category: SPINE, Structural Proteomics in Europe]]
Retrieved from "https://proteopedia.org/2ew9"