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==Solution structure of domains 3 and 4 of human ATP7B==
==Solution structure of domains 3 and 4 of human ATP7B==
<StructureSection load='2rop' size='340' side='right'caption='[[2rop]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
<StructureSection load='2rop' size='340' side='right'caption='[[2rop]]' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2rop]] 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=2ROP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ROP FirstGlance]. <br>
<table><tr><td colspan='2'>[[2rop]] 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=2ROP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ROP FirstGlance]. <br>
</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">ATP7B ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2rop FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2rop OCA], [https://pdbe.org/2rop PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2rop RCSB], [https://www.ebi.ac.uk/pdbsum/2rop PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2rop ProSAT]</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'>[https://proteopedia.org/fgij/fg.htm?mol=2rop FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2rop OCA], [https://pdbe.org/2rop PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2rop RCSB], [https://www.ebi.ac.uk/pdbsum/2rop PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2rop ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[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>
[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 ==
[[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.  
[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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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Copper-exporting ATPase]]
[[Category: Homo sapiens]]
[[Category: Human]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Banci, L]]
[[Category: Banci L]]
[[Category: Bertini, I]]
[[Category: Bertini I]]
[[Category: Cantini, F]]
[[Category: Cantini F]]
[[Category: Rosenzweig, A C]]
[[Category: Rosenzweig AC]]
[[Category: Yatsunyk, L A]]
[[Category: Yatsunyk LA]]
[[Category: Alternative splicing]]
[[Category: Atp-binding]]
[[Category: Copper]]
[[Category: Copper transport]]
[[Category: Cytoplasm]]
[[Category: Disease mutation]]
[[Category: Golgi apparatus]]
[[Category: Hydrolase]]
[[Category: Ion transport]]
[[Category: Magnesium]]
[[Category: Membrane]]
[[Category: Metal-binding]]
[[Category: Mitochondrion]]
[[Category: Mobility]]
[[Category: Nucleotide-binding]]
[[Category: Phosphoprotein]]
[[Category: Polymorphism]]
[[Category: Protein-protein interaction]]
[[Category: Transmembrane]]
[[Category: Transport]]
[[Category: Wilson protein]]
Retrieved from "https://proteopedia.org/2rop"