Actions of a picomolar short-acting S1P1 agonist in S1P1-eGFP knock-in mice
A selective, short-acting agonist for the sphingosine-1-phosphate receptor S1P 1 and GFP-S1P 1 knock-in mouse model are used to show that both receptor degradation and receptor reserve underlie the mechanisms of lymphocyte sequestration by agonists. Sphingosine 1-phosphate receptor 1 (S1P 1 ) is cri...
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| Veröffentlicht in: | Nature chemical biology 2011-05, Vol.7 (5), p.254-256 |
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| creator | Cahalan, Stuart M Gonzalez-Cabrera, Pedro J Sarkisyan, Gor Nguyen, Nhan Schaeffer, Marie-Therese Huang, Liming Yeager, Adam Clemons, Bryan Scott, Fiona Rosen, Hugh |
| description | A selective, short-acting agonist for the sphingosine-1-phosphate receptor S1P
1
and GFP-S1P
1
knock-in mouse model are used to show that both receptor degradation and receptor reserve underlie the mechanisms of lymphocyte sequestration by agonists.
Sphingosine 1-phosphate receptor 1 (S1P
1
) is critical for lymphocyte recirculation and is a clinical target for treatment of multiple sclerosis. By generating a short-duration S1P
1
agonist and mice in which fluorescently tagged S1P
1
replaces wild-type receptor, we elucidate physiological and agonist-perturbed changes in expression of S1P
1
at a subcellular level
in vivo
. We demonstrate differential downregulation of S1P
1
on lymphocytes and endothelia after agonist treatment. |
| doi_str_mv | 10.1038/nchembio.547 |
| format | Article |
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1
and GFP-S1P
1
knock-in mouse model are used to show that both receptor degradation and receptor reserve underlie the mechanisms of lymphocyte sequestration by agonists.
Sphingosine 1-phosphate receptor 1 (S1P
1
) is critical for lymphocyte recirculation and is a clinical target for treatment of multiple sclerosis. By generating a short-duration S1P
1
agonist and mice in which fluorescently tagged S1P
1
replaces wild-type receptor, we elucidate physiological and agonist-perturbed changes in expression of S1P
1
at a subcellular level
in vivo
. We demonstrate differential downregulation of S1P
1
on lymphocytes and endothelia after agonist treatment.</description><identifier>ISSN: 1552-4450</identifier><identifier>EISSN: 1552-4469</identifier><identifier>DOI: 10.1038/nchembio.547</identifier><identifier>PMID: 21445057</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/1619 ; 631/92/609 ; 692/699/249/1313/1666 ; Animals ; Biochemical Engineering ; Biochemistry ; Bioorganic Chemistry ; brief-communication ; Cell Biology ; Cellular biology ; Chemistry ; Chemistry and Materials Science ; Chemistry/Food Science ; Down-Regulation - drug effects ; Endothelium - drug effects ; Endothelium - metabolism ; Flow Cytometry ; Fluorescent Dyes - chemistry ; Fluorescent Dyes - metabolism ; Gene expression ; Gene Knock-In Techniques ; Green Fluorescent Proteins - chemistry ; Green Fluorescent Proteins - metabolism ; Lymphocytes ; Lymphocytes - drug effects ; Lymphocytes - metabolism ; Mice ; Multiple sclerosis ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - metabolism ; Multiple Sclerosis - pathology ; Physiology ; Receptors, Lysosphingolipid - agonists ; Receptors, Lysosphingolipid - metabolism ; Receptors, Lysosphingolipid - therapeutic use ; Rodents ; Time Factors</subject><ispartof>Nature chemical biology, 2011-05, Vol.7 (5), p.254-256</ispartof><rights>Springer Nature America, Inc. 2011</rights><rights>Copyright Nature Publishing Group May 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3597-ce51187e6ed4072cce145ea40de7094e83b167b355cc98fdc9c5cbc019e53e793</citedby><cites>FETCH-LOGICAL-c3597-ce51187e6ed4072cce145ea40de7094e83b167b355cc98fdc9c5cbc019e53e793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nchembio.547$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nchembio.547$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27915,27916,41479,42548,51310</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21445057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cahalan, Stuart M</creatorcontrib><creatorcontrib>Gonzalez-Cabrera, Pedro J</creatorcontrib><creatorcontrib>Sarkisyan, Gor</creatorcontrib><creatorcontrib>Nguyen, Nhan</creatorcontrib><creatorcontrib>Schaeffer, Marie-Therese</creatorcontrib><creatorcontrib>Huang, Liming</creatorcontrib><creatorcontrib>Yeager, Adam</creatorcontrib><creatorcontrib>Clemons, Bryan</creatorcontrib><creatorcontrib>Scott, Fiona</creatorcontrib><creatorcontrib>Rosen, Hugh</creatorcontrib><title>Actions of a picomolar short-acting S1P1 agonist in S1P1-eGFP knock-in mice</title><title>Nature chemical biology</title><addtitle>Nat Chem Biol</addtitle><addtitle>Nat Chem Biol</addtitle><description>A selective, short-acting agonist for the sphingosine-1-phosphate receptor S1P
1
and GFP-S1P
1
knock-in mouse model are used to show that both receptor degradation and receptor reserve underlie the mechanisms of lymphocyte sequestration by agonists.
Sphingosine 1-phosphate receptor 1 (S1P
1
) is critical for lymphocyte recirculation and is a clinical target for treatment of multiple sclerosis. By generating a short-duration S1P
1
agonist and mice in which fluorescently tagged S1P
1
replaces wild-type receptor, we elucidate physiological and agonist-perturbed changes in expression of S1P
1
at a subcellular level
in vivo
. We demonstrate differential downregulation of S1P
1
on lymphocytes and endothelia after agonist treatment.</description><subject>631/250/1619</subject><subject>631/92/609</subject><subject>692/699/249/1313/1666</subject><subject>Animals</subject><subject>Biochemical Engineering</subject><subject>Biochemistry</subject><subject>Bioorganic Chemistry</subject><subject>brief-communication</subject><subject>Cell Biology</subject><subject>Cellular biology</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Chemistry/Food Science</subject><subject>Down-Regulation - drug effects</subject><subject>Endothelium - drug effects</subject><subject>Endothelium - metabolism</subject><subject>Flow Cytometry</subject><subject>Fluorescent Dyes - chemistry</subject><subject>Fluorescent Dyes - metabolism</subject><subject>Gene expression</subject><subject>Gene Knock-In Techniques</subject><subject>Green Fluorescent Proteins - chemistry</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Lymphocytes</subject><subject>Lymphocytes - drug effects</subject><subject>Lymphocytes - metabolism</subject><subject>Mice</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - drug therapy</subject><subject>Multiple Sclerosis - metabolism</subject><subject>Multiple Sclerosis - pathology</subject><subject>Physiology</subject><subject>Receptors, Lysosphingolipid - agonists</subject><subject>Receptors, Lysosphingolipid - metabolism</subject><subject>Receptors, Lysosphingolipid - therapeutic use</subject><subject>Rodents</subject><subject>Time 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Biol</addtitle><date>2011-05</date><risdate>2011</risdate><volume>7</volume><issue>5</issue><spage>254</spage><epage>256</epage><pages>254-256</pages><issn>1552-4450</issn><eissn>1552-4469</eissn><abstract>A selective, short-acting agonist for the sphingosine-1-phosphate receptor S1P
1
and GFP-S1P
1
knock-in mouse model are used to show that both receptor degradation and receptor reserve underlie the mechanisms of lymphocyte sequestration by agonists.
Sphingosine 1-phosphate receptor 1 (S1P
1
) is critical for lymphocyte recirculation and is a clinical target for treatment of multiple sclerosis. By generating a short-duration S1P
1
agonist and mice in which fluorescently tagged S1P
1
replaces wild-type receptor, we elucidate physiological and agonist-perturbed changes in expression of S1P
1
at a subcellular level
in vivo
. We demonstrate differential downregulation of S1P
1
on lymphocytes and endothelia after agonist treatment.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>21445057</pmid><doi>10.1038/nchembio.547</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature chemical biology, 2011-05, Vol.7 (5), p.254-256 |
| issn | 1552-4450 1552-4469 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3430385 |
| source | MEDLINE; Nature Research; SpringerLink Journals - AutoHoldings |
| subjects | 631/250/1619 631/92/609 692/699/249/1313/1666 Animals Biochemical Engineering Biochemistry Bioorganic Chemistry brief-communication Cell Biology Cellular biology Chemistry Chemistry and Materials Science Chemistry/Food Science Down-Regulation - drug effects Endothelium - drug effects Endothelium - metabolism Flow Cytometry Fluorescent Dyes - chemistry Fluorescent Dyes - metabolism Gene expression Gene Knock-In Techniques Green Fluorescent Proteins - chemistry Green Fluorescent Proteins - metabolism Lymphocytes Lymphocytes - drug effects Lymphocytes - metabolism Mice Multiple sclerosis Multiple Sclerosis - drug therapy Multiple Sclerosis - metabolism Multiple Sclerosis - pathology Physiology Receptors, Lysosphingolipid - agonists Receptors, Lysosphingolipid - metabolism Receptors, Lysosphingolipid - therapeutic use Rodents Time Factors |
| title | Actions of a picomolar short-acting S1P1 agonist in S1P1-eGFP knock-in mice |
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