2mkv

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'''Unreleased structure'''
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==Structure of the NA,K-ATPASE regulatory protein FXYD2b in micelles==
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<StructureSection load='2mkv' size='340' side='right' caption='[[2mkv]], [[NMR_Ensembles_of_Models | 10 NMR models]]' scene=''>
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The entry 2mkv is ON HOLD
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== Structural highlights ==
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<table><tr><td colspan='2'>[[2mkv]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MKV OCA]. <br>
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Authors: Marassi, F.M., Gong, X.
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</td></tr><tr><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2jo1|2jo1]], [[2jp3|2jp3]]</td></tr>
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<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </span></td></tr>
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Description: Structure of the NA,K-ATPASE regulatory protein FXYD2b in micelles
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<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2mkv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mkv OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2mkv RCSB], [http://www.ebi.ac.uk/pdbsum/2mkv PDBsum]</span></td></tr>
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<table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/ATNG_HUMAN ATNG_HUMAN]] Autosomal dominant primary hypomagnesemia with hypocalcuria. The disease is caused by mutations affecting the gene represented in this entry.
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== Function ==
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[[http://www.uniprot.org/uniprot/ATNG_HUMAN ATNG_HUMAN]] May be involved in forming the receptor site for cardiac glycoside binding or may modulate the transport function of the sodium ATPase.
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__TOC__
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</StructureSection>
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[[Category: Gong, X.]]
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[[Category: Marassi, F M.]]
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[[Category: Fxyd]]
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[[Category: Fxyd2b]]
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[[Category: K-atpase]]
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[[Category: Micelle]]
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[[Category: Na]]
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[[Category: Transport protein]]

Revision as of 07:21, 14 May 2014

Structure of the NA,K-ATPASE regulatory protein FXYD2b in micelles

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