Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84
Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules related to 3,3′-diindolylmethane. 3,3′-Diindolylmethane and decanoic acid acted as strong positive allosteric modulators of the function of each other and analysis showed the affinity of 3,3′-diindoly...
Gespeichert in:
Veröffentlicht in: | Scientific reports 2017-12, Vol.7 (1), p.17953-15, Article 17953 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 15 |
---|---|
container_issue | 1 |
container_start_page | 17953 |
container_title | Scientific reports |
container_volume | 7 |
creator | Mahmud, Zobaer Al Jenkins, Laura Ulven, Trond Labéguère, Frédéric Gosmini, Romain De Vos, Steve Hudson, Brian D. Tikhonova, Irina G. Milligan, Graeme |
description | Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules related to 3,3′-diindolylmethane. 3,3′-Diindolylmethane and decanoic acid acted as strong positive allosteric modulators of the function of each other and analysis showed the affinity of 3,3′-diindolylmethane to be at least 100 fold higher. Methyl decanoate was not an agonist at GPR84. This implies a key role in binding for the carboxylic acid of the fatty acid. Via homology modelling we predicted and confirmed an integral role of arginine
172
, located in the 2nd extracellular loop, in the action of decanoic acid but not of 3,3′-diindolylmethane. Exemplars from a patented series of GPR84 antagonists were able to block agonist actions of both decanoic acid and 3,3′-diindolylmethane at GPR84. However, although a radiolabelled form of a related antagonist, [
3
H]G9543, was able to bind with high affinity to GPR84, this was not competed for by increasing concentrations of either decanoic acid or 3,3′
-
diindolylmethane and was not affected adversely by mutation of arginine
172
. These studies identify three separable ligand binding sites within GPR84 and suggest that if medium chain fatty acids are true endogenous regulators then co-binding with a positive allosteric modulator would greatly enhance their function in physiological settings. |
doi_str_mv | 10.1038/s41598-017-18159-3 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5738391</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1983424589</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-5accd9c7944ba212b92c917cf1e70868078220bfc05c8f4bf016ff8e9b4d2c2d3</originalsourceid><addsrcrecordid>eNp1kU1rFTEUhoMottT-gS4k4MbNaD7vJBtBSr0KBUXadchkTu6kzE3GJCP475t6a7kKZpMD5zlvcngQuqDkHSVcvS-CSq06QvuOqlZ2_Bk6ZUTIjnHGnh_VJ-i8lDvSjmRaUP0SnTDNNlwQcorczZQBsJttKVBw8ngOOxvHgsG6CQ8hjrgmPIZSQ3QVl1AfsIjrBDjlZbIRb_GSU4UQO5fWZYYRZ3Cw1JTx9tt3JV6hF97OBc4f7zN0--nq5vJzd_11--Xy43XnRC9qJ61zo3a9FmKwjLJBM6dp7zyFnqiNIr1ijAzeEemUF4MndOO9Aj2IkTk28jP04ZC7rMMeRgexZjubJYe9zb9MssH83YlhMrv008ieK65pC3j7GJDTjxVKNftQHMyzjZDWYqjutSSCcdnQN_-gd2nNsa3XKMUFE1LpRrED5XIqJYN_-gwl5kGjOWg0TaP5rdHwNvT6eI2nkT_SGsAPQGmtuIN89Pb_Y-8BlEuomA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1983424589</pqid></control><display><type>article</type><title>Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Springer Nature OA Free Journals</source><source>Nature Free</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Mahmud, Zobaer Al ; Jenkins, Laura ; Ulven, Trond ; Labéguère, Frédéric ; Gosmini, Romain ; De Vos, Steve ; Hudson, Brian D. ; Tikhonova, Irina G. ; Milligan, Graeme</creator><creatorcontrib>Mahmud, Zobaer Al ; Jenkins, Laura ; Ulven, Trond ; Labéguère, Frédéric ; Gosmini, Romain ; De Vos, Steve ; Hudson, Brian D. ; Tikhonova, Irina G. ; Milligan, Graeme</creatorcontrib><description>Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules related to 3,3′-diindolylmethane. 3,3′-Diindolylmethane and decanoic acid acted as strong positive allosteric modulators of the function of each other and analysis showed the affinity of 3,3′-diindolylmethane to be at least 100 fold higher. Methyl decanoate was not an agonist at GPR84. This implies a key role in binding for the carboxylic acid of the fatty acid. Via homology modelling we predicted and confirmed an integral role of arginine
172
, located in the 2nd extracellular loop, in the action of decanoic acid but not of 3,3′-diindolylmethane. Exemplars from a patented series of GPR84 antagonists were able to block agonist actions of both decanoic acid and 3,3′-diindolylmethane at GPR84. However, although a radiolabelled form of a related antagonist, [
3
H]G9543, was able to bind with high affinity to GPR84, this was not competed for by increasing concentrations of either decanoic acid or 3,3′
-
diindolylmethane and was not affected adversely by mutation of arginine
172
. These studies identify three separable ligand binding sites within GPR84 and suggest that if medium chain fatty acids are true endogenous regulators then co-binding with a positive allosteric modulator would greatly enhance their function in physiological settings.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-18159-3</identifier><identifier>PMID: 29263400</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/154 ; 631/154/436 ; 631/92 ; 96 ; 96/95 ; Affinity ; Allosteric properties ; Binding Sites ; Carboxylic acids ; Decanoic Acids - metabolism ; Fatty acids ; Homology ; Humanities and Social Sciences ; Humans ; Indoles - metabolism ; Inflammation ; Ligands ; multidisciplinary ; Receptors, Cell Surface - metabolism ; Science ; Science (multidisciplinary) ; Structure-Activity Relationship</subject><ispartof>Scientific reports, 2017-12, Vol.7 (1), p.17953-15, Article 17953</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-5accd9c7944ba212b92c917cf1e70868078220bfc05c8f4bf016ff8e9b4d2c2d3</citedby><cites>FETCH-LOGICAL-c474t-5accd9c7944ba212b92c917cf1e70868078220bfc05c8f4bf016ff8e9b4d2c2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738391/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738391/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29263400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mahmud, Zobaer Al</creatorcontrib><creatorcontrib>Jenkins, Laura</creatorcontrib><creatorcontrib>Ulven, Trond</creatorcontrib><creatorcontrib>Labéguère, Frédéric</creatorcontrib><creatorcontrib>Gosmini, Romain</creatorcontrib><creatorcontrib>De Vos, Steve</creatorcontrib><creatorcontrib>Hudson, Brian D.</creatorcontrib><creatorcontrib>Tikhonova, Irina G.</creatorcontrib><creatorcontrib>Milligan, Graeme</creatorcontrib><title>Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules related to 3,3′-diindolylmethane. 3,3′-Diindolylmethane and decanoic acid acted as strong positive allosteric modulators of the function of each other and analysis showed the affinity of 3,3′-diindolylmethane to be at least 100 fold higher. Methyl decanoate was not an agonist at GPR84. This implies a key role in binding for the carboxylic acid of the fatty acid. Via homology modelling we predicted and confirmed an integral role of arginine
172
, located in the 2nd extracellular loop, in the action of decanoic acid but not of 3,3′-diindolylmethane. Exemplars from a patented series of GPR84 antagonists were able to block agonist actions of both decanoic acid and 3,3′-diindolylmethane at GPR84. However, although a radiolabelled form of a related antagonist, [
3
H]G9543, was able to bind with high affinity to GPR84, this was not competed for by increasing concentrations of either decanoic acid or 3,3′
-
diindolylmethane and was not affected adversely by mutation of arginine
172
. These studies identify three separable ligand binding sites within GPR84 and suggest that if medium chain fatty acids are true endogenous regulators then co-binding with a positive allosteric modulator would greatly enhance their function in physiological settings.</description><subject>631/154</subject><subject>631/154/436</subject><subject>631/92</subject><subject>96</subject><subject>96/95</subject><subject>Affinity</subject><subject>Allosteric properties</subject><subject>Binding Sites</subject><subject>Carboxylic acids</subject><subject>Decanoic Acids - metabolism</subject><subject>Fatty acids</subject><subject>Homology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Indoles - metabolism</subject><subject>Inflammation</subject><subject>Ligands</subject><subject>multidisciplinary</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Structure-Activity Relationship</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1rFTEUhoMottT-gS4k4MbNaD7vJBtBSr0KBUXadchkTu6kzE3GJCP475t6a7kKZpMD5zlvcngQuqDkHSVcvS-CSq06QvuOqlZ2_Bk6ZUTIjnHGnh_VJ-i8lDvSjmRaUP0SnTDNNlwQcorczZQBsJttKVBw8ngOOxvHgsG6CQ8hjrgmPIZSQ3QVl1AfsIjrBDjlZbIRb_GSU4UQO5fWZYYRZ3Cw1JTx9tt3JV6hF97OBc4f7zN0--nq5vJzd_11--Xy43XnRC9qJ61zo3a9FmKwjLJBM6dp7zyFnqiNIr1ijAzeEemUF4MndOO9Aj2IkTk28jP04ZC7rMMeRgexZjubJYe9zb9MssH83YlhMrv008ieK65pC3j7GJDTjxVKNftQHMyzjZDWYqjutSSCcdnQN_-gd2nNsa3XKMUFE1LpRrED5XIqJYN_-gwl5kGjOWg0TaP5rdHwNvT6eI2nkT_SGsAPQGmtuIN89Pb_Y-8BlEuomA</recordid><startdate>20171220</startdate><enddate>20171220</enddate><creator>Mahmud, Zobaer Al</creator><creator>Jenkins, Laura</creator><creator>Ulven, Trond</creator><creator>Labéguère, Frédéric</creator><creator>Gosmini, Romain</creator><creator>De Vos, Steve</creator><creator>Hudson, Brian D.</creator><creator>Tikhonova, Irina G.</creator><creator>Milligan, Graeme</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171220</creationdate><title>Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84</title><author>Mahmud, Zobaer Al ; Jenkins, Laura ; Ulven, Trond ; Labéguère, Frédéric ; Gosmini, Romain ; De Vos, Steve ; Hudson, Brian D. ; Tikhonova, Irina G. ; Milligan, Graeme</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-5accd9c7944ba212b92c917cf1e70868078220bfc05c8f4bf016ff8e9b4d2c2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>631/154</topic><topic>631/154/436</topic><topic>631/92</topic><topic>96</topic><topic>96/95</topic><topic>Affinity</topic><topic>Allosteric properties</topic><topic>Binding Sites</topic><topic>Carboxylic acids</topic><topic>Decanoic Acids - metabolism</topic><topic>Fatty acids</topic><topic>Homology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Indoles - metabolism</topic><topic>Inflammation</topic><topic>Ligands</topic><topic>multidisciplinary</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Structure-Activity Relationship</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mahmud, Zobaer Al</creatorcontrib><creatorcontrib>Jenkins, Laura</creatorcontrib><creatorcontrib>Ulven, Trond</creatorcontrib><creatorcontrib>Labéguère, Frédéric</creatorcontrib><creatorcontrib>Gosmini, Romain</creatorcontrib><creatorcontrib>De Vos, Steve</creatorcontrib><creatorcontrib>Hudson, Brian D.</creatorcontrib><creatorcontrib>Tikhonova, Irina G.</creatorcontrib><creatorcontrib>Milligan, Graeme</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mahmud, Zobaer Al</au><au>Jenkins, Laura</au><au>Ulven, Trond</au><au>Labéguère, Frédéric</au><au>Gosmini, Romain</au><au>De Vos, Steve</au><au>Hudson, Brian D.</au><au>Tikhonova, Irina G.</au><au>Milligan, Graeme</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-12-20</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>17953</spage><epage>15</epage><pages>17953-15</pages><artnum>17953</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules related to 3,3′-diindolylmethane. 3,3′-Diindolylmethane and decanoic acid acted as strong positive allosteric modulators of the function of each other and analysis showed the affinity of 3,3′-diindolylmethane to be at least 100 fold higher. Methyl decanoate was not an agonist at GPR84. This implies a key role in binding for the carboxylic acid of the fatty acid. Via homology modelling we predicted and confirmed an integral role of arginine
172
, located in the 2nd extracellular loop, in the action of decanoic acid but not of 3,3′-diindolylmethane. Exemplars from a patented series of GPR84 antagonists were able to block agonist actions of both decanoic acid and 3,3′-diindolylmethane at GPR84. However, although a radiolabelled form of a related antagonist, [
3
H]G9543, was able to bind with high affinity to GPR84, this was not competed for by increasing concentrations of either decanoic acid or 3,3′
-
diindolylmethane and was not affected adversely by mutation of arginine
172
. These studies identify three separable ligand binding sites within GPR84 and suggest that if medium chain fatty acids are true endogenous regulators then co-binding with a positive allosteric modulator would greatly enhance their function in physiological settings.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29263400</pmid><doi>10.1038/s41598-017-18159-3</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2045-2322 |
ispartof | Scientific reports, 2017-12, Vol.7 (1), p.17953-15, Article 17953 |
issn | 2045-2322 2045-2322 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5738391 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | 631/154 631/154/436 631/92 96 96/95 Affinity Allosteric properties Binding Sites Carboxylic acids Decanoic Acids - metabolism Fatty acids Homology Humanities and Social Sciences Humans Indoles - metabolism Inflammation Ligands multidisciplinary Receptors, Cell Surface - metabolism Science Science (multidisciplinary) Structure-Activity Relationship |
title | Three classes of ligands each bind to distinct sites on the orphan G protein-coupled receptor GPR84 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T02%3A57%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Three%20classes%20of%20ligands%20each%20bind%20to%20distinct%20sites%20on%20the%20orphan%20G%20protein-coupled%20receptor%20GPR84&rft.jtitle=Scientific%20reports&rft.au=Mahmud,%20Zobaer%20Al&rft.date=2017-12-20&rft.volume=7&rft.issue=1&rft.spage=17953&rft.epage=15&rft.pages=17953-15&rft.artnum=17953&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-017-18159-3&rft_dat=%3Cproquest_pubme%3E1983424589%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1983424589&rft_id=info:pmid/29263400&rfr_iscdi=true |