2n2f

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<StructureSection load='2n2f' size='340' side='right'caption='[[2n2f]], [[NMR_Ensembles_of_Models | 10 NMR models]]' scene=''>
<StructureSection load='2n2f' size='340' side='right'caption='[[2n2f]], [[NMR_Ensembles_of_Models | 10 NMR models]]' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[2n2f]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2N2F OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2N2F FirstGlance]. <br>
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<table><tr><td colspan='2'>[[2n2f]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2N2F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N2F FirstGlance]. <br>
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</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=2n2f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n2f OCA], [http://pdbe.org/2n2f PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2n2f RCSB], [http://www.ebi.ac.uk/pdbsum/2n2f PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2n2f ProSAT]</span></td></tr>
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</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=2n2f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n2f OCA], [https://pdbe.org/2n2f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n2f RCSB], [https://www.ebi.ac.uk/pdbsum/2n2f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n2f ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
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[[http://www.uniprot.org/uniprot/PDYN_HUMAN PDYN_HUMAN]] Spinocerebellar ataxia type 23. The disease is caused by mutations affecting the gene represented in this entry.
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[[https://www.uniprot.org/uniprot/PDYN_HUMAN PDYN_HUMAN]] Spinocerebellar ataxia type 23. The disease is caused by mutations affecting the gene represented in this entry.
== Function ==
== Function ==
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[[http://www.uniprot.org/uniprot/PDYN_HUMAN PDYN_HUMAN]] Leu-enkephalins compete with and mimic the effects of opiate drugs. They play a role in a number of physiologic functions, including pain perception and responses to stress (By similarity). Dynorphin peptides differentially regulate the kappa opioid receptor. Dynorphin A(1-13) has a typical opiod activity, it is 700 times more potent than Leu-enkephalin (By similarity). Leumorphin has a typical opiod activity and may have anti-apoptotic effect.
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[[https://www.uniprot.org/uniprot/PDYN_HUMAN PDYN_HUMAN]] Leu-enkephalins compete with and mimic the effects of opiate drugs. They play a role in a number of physiologic functions, including pain perception and responses to stress (By similarity). Dynorphin peptides differentially regulate the kappa opioid receptor. Dynorphin A(1-13) has a typical opiod activity, it is 700 times more potent than Leu-enkephalin (By similarity). Leumorphin has a typical opiod activity and may have anti-apoptotic effect.
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==

Revision as of 09:04, 23 February 2022

Solution NMR structure of Dynorphin 1-13 bound to Kappa Opioid Receptor

PDB ID 2n2f

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