7y1f: Difference between revisions

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== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[7y1f]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Y1F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Y1F FirstGlance]. <br>
<table><tr><td colspan='2'>[[7y1f]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7Y1F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7Y1F 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=7y1f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7y1f OCA], [https://pdbe.org/7y1f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7y1f RCSB], [https://www.ebi.ac.uk/pdbsum/7y1f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7y1f ProSAT]</span></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.3&#8491;</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=7y1f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7y1f OCA], [https://pdbe.org/7y1f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7y1f RCSB], [https://www.ebi.ac.uk/pdbsum/7y1f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7y1f ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
[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 ==
[https://www.uniprot.org/uniprot/OPRK_HUMAN OPRK_HUMAN] G-protein coupled opioid receptor that functions as receptor for endogenous alpha-neoendorphins and dynorphins, but has low affinity for beta-endorphins. Also functions as receptor for various synthetic opioids and for the psychoactive diterpene salvinorin A. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain. Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions.<ref>PMID:12004055</ref> <ref>PMID:22437504</ref> <ref>PMID:7624359</ref> <ref>PMID:8060324</ref>
[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.
== References ==
 
<references/>
==See Also==
*[[Opioid receptor|Opioid receptor]]
*[[Transducin 3D structures|Transducin 3D structures]]
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</StructureSection>
</StructureSection>

Latest revision as of 14:45, 23 October 2024

Cryo-EM structure of human k-opioid receptor-Gi complexCryo-EM structure of human k-opioid receptor-Gi complex

Structural highlights

7y1f is a 6 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:Electron Microscopy, Resolution 3.3Å
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

PDYN_HUMAN Spinocerebellar ataxia type 23. The disease is caused by mutations affecting the gene represented in this entry.

Function

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.

See Also

7y1f, resolution 3.30Å

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