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The Roles of Lpar1 in Central Nervous System Disorders and Diseases
Lysophosphatidic acid receptor 1 (Lpar1) , which is found in almost all human tissues but is most abundant in the brain, can couple to G protein-coupled receptors (GPCRs) and participate in regulating cell proliferation, migration, survival, and apoptosis. Endothelial differentiation gene-2 receptor...
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Published in: | Frontiers in neuroscience 2021-07, Vol.15, p.710473-710473 |
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description | Lysophosphatidic acid receptor 1 (Lpar1) , which is found in almost all human tissues but is most abundant in the brain, can couple to G protein-coupled receptors (GPCRs) and participate in regulating cell proliferation, migration, survival, and apoptosis. Endothelial differentiation gene-2 receptor (Edg2), the protein encoded by the Lpar1 gene, is present on various cell types in the central nervous system (CNS), such as neural stem cells (NSCs), oligodendrocytes, neurons, astrocytes, and microglia. Lpar1 deletion causes neurodevelopmental disorders and CNS diseases, such as brain cancer, neuropsychiatric disorders, demyelination diseases, and neuropathic pain. Here, we summarize the possible roles and mechanisms of Lpar1/ Edg2 in CNS disorders and diseases and propose that Lpar1/ Edg2 might be a potential therapeutic target for CNS disorders and diseases. |
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Endothelial differentiation gene-2 receptor (Edg2), the protein encoded by the Lpar1 gene, is present on various cell types in the central nervous system (CNS), such as neural stem cells (NSCs), oligodendrocytes, neurons, astrocytes, and microglia. Lpar1 deletion causes neurodevelopmental disorders and CNS diseases, such as brain cancer, neuropsychiatric disorders, demyelination diseases, and neuropathic pain. Here, we summarize the possible roles and mechanisms of Lpar1/ Edg2 in CNS disorders and diseases and propose that Lpar1/ Edg2 might be a potential therapeutic target for CNS disorders and diseases.</description><identifier>ISSN: 1662-453X</identifier><identifier>ISSN: 1662-4548</identifier><identifier>EISSN: 1662-453X</identifier><identifier>DOI: 10.3389/fnins.2021.710473</identifier><identifier>PMID: 34385905</identifier><language>eng</language><publisher>Lausanne: Frontiers Research Foundation</publisher><subject>Apoptosis ; astrocyte ; Astrocytes ; astroglia ; Binding sites ; Biosynthesis ; Brain ; Cell cycle ; Cell migration ; Cell proliferation ; Cell survival ; Central nervous system ; Demyelination ; Edg2 ; Endoplasmic reticulum ; G protein-coupled receptors ; Kinases ; Ligands ; Lpar1 ; Lysophosphatidic acid ; Mental disorders ; Microglia ; Morphology ; Mutation ; Nervous system ; Neural stem cells ; Neuralgia ; Neurodevelopmental disorders ; Neurogenesis ; Neuroscience ; oligodendrocyte ; Oligodendrocytes ; Proteins ; Roles ; Stem cells ; Therapeutic targets</subject><ispartof>Frontiers in neuroscience, 2021-07, Vol.15, p.710473-710473</ispartof><rights>2021. This work is licensed 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><rights>Copyright © 2021 Xiao, Su, Gao, Li and Qu. 2021 Xiao, Su, Gao, Li and Qu</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-6f48412feefc006875d0a524536cb04373a429d4bfa9f087fb844bb505040ee3</citedby><cites>FETCH-LOGICAL-c470t-6f48412feefc006875d0a524536cb04373a429d4bfa9f087fb844bb505040ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2555481749/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2555481749?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids></links><search><creatorcontrib>Xiao, Dongqiong</creatorcontrib><creatorcontrib>Su, Xiaojuan</creatorcontrib><creatorcontrib>Gao, Hu</creatorcontrib><creatorcontrib>Li, Xihong</creatorcontrib><creatorcontrib>Qu, Yi</creatorcontrib><title>The Roles of Lpar1 in Central Nervous System Disorders and Diseases</title><title>Frontiers in neuroscience</title><description>Lysophosphatidic acid receptor 1 (Lpar1) , which is found in almost all human tissues but is most abundant in the brain, can couple to G protein-coupled receptors (GPCRs) and participate in regulating cell proliferation, migration, survival, and apoptosis. Endothelial differentiation gene-2 receptor (Edg2), the protein encoded by the Lpar1 gene, is present on various cell types in the central nervous system (CNS), such as neural stem cells (NSCs), oligodendrocytes, neurons, astrocytes, and microglia. Lpar1 deletion causes neurodevelopmental disorders and CNS diseases, such as brain cancer, neuropsychiatric disorders, demyelination diseases, and neuropathic pain. Here, we summarize the possible roles and mechanisms of Lpar1/ Edg2 in CNS disorders and diseases and propose that Lpar1/ Edg2 might be a potential therapeutic target for CNS disorders and diseases.</description><subject>Apoptosis</subject><subject>astrocyte</subject><subject>Astrocytes</subject><subject>astroglia</subject><subject>Binding sites</subject><subject>Biosynthesis</subject><subject>Brain</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cell survival</subject><subject>Central nervous system</subject><subject>Demyelination</subject><subject>Edg2</subject><subject>Endoplasmic reticulum</subject><subject>G protein-coupled receptors</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lpar1</subject><subject>Lysophosphatidic acid</subject><subject>Mental disorders</subject><subject>Microglia</subject><subject>Morphology</subject><subject>Mutation</subject><subject>Nervous system</subject><subject>Neural stem cells</subject><subject>Neuralgia</subject><subject>Neurodevelopmental disorders</subject><subject>Neurogenesis</subject><subject>Neuroscience</subject><subject>oligodendrocyte</subject><subject>Oligodendrocytes</subject><subject>Proteins</subject><subject>Roles</subject><subject>Stem cells</subject><subject>Therapeutic targets</subject><issn>1662-453X</issn><issn>1662-4548</issn><issn>1662-453X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkUtPGzEUha0KVF79Ad1Z6oZNgh_XY8-mUpU-QIpAgiy6s-yZa5hoMk7tCRL_HodBFbCyfX303XPvIeQrZ3MpTX0Rhm7Ic8EEn2vOQMtP5JhXlZiBkn8P3tyPyEnOa8YqYUB8JkcSpFE1U8dksXpAeht7zDQGuty6xGk30AUOY3I9vcb0GHeZ3j3lETf0Z5djajFl6oZ2_0KXMZ-Rw-D6jF9ez1Oy-v1rtbicLW_-XC1-LGcNaDbOqgAGuAiIoSlWjFYtc0oUf1XjGUgtHYi6BR9cHZjRwRsA7xVTDBiiPCVXE7aNbm23qdu49GSj6-xLIaZ769LYNT3a0qBumQCuvYDSxRuvpaylBNNIVbvC-j6xtju_wbaZxn0Hff8zdA_2Pj5aI5UUShfA-SsgxX87zKPddLnBvncDloVZoSpexhVQFem3D9J13KWhbKqolALDNdRFxSdVk2LOCcN_M5zZfdr2JW27T9tOactnIISbNQ</recordid><startdate>20210727</startdate><enddate>20210727</enddate><creator>Xiao, Dongqiong</creator><creator>Su, Xiaojuan</creator><creator>Gao, Hu</creator><creator>Li, Xihong</creator><creator>Qu, Yi</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20210727</creationdate><title>The Roles of Lpar1 in Central Nervous System Disorders and Diseases</title><author>Xiao, Dongqiong ; Su, Xiaojuan ; Gao, Hu ; Li, Xihong ; Qu, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-6f48412feefc006875d0a524536cb04373a429d4bfa9f087fb844bb505040ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>astrocyte</topic><topic>Astrocytes</topic><topic>astroglia</topic><topic>Binding sites</topic><topic>Biosynthesis</topic><topic>Brain</topic><topic>Cell cycle</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cell survival</topic><topic>Central nervous system</topic><topic>Demyelination</topic><topic>Edg2</topic><topic>Endoplasmic reticulum</topic><topic>G protein-coupled receptors</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Lpar1</topic><topic>Lysophosphatidic acid</topic><topic>Mental disorders</topic><topic>Microglia</topic><topic>Morphology</topic><topic>Mutation</topic><topic>Nervous system</topic><topic>Neural stem cells</topic><topic>Neuralgia</topic><topic>Neurodevelopmental disorders</topic><topic>Neurogenesis</topic><topic>Neuroscience</topic><topic>oligodendrocyte</topic><topic>Oligodendrocytes</topic><topic>Proteins</topic><topic>Roles</topic><topic>Stem cells</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Dongqiong</creatorcontrib><creatorcontrib>Su, Xiaojuan</creatorcontrib><creatorcontrib>Gao, Hu</creatorcontrib><creatorcontrib>Li, Xihong</creatorcontrib><creatorcontrib>Qu, Yi</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content (ProQuest)</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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Frontiers in neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Dongqiong</au><au>Su, Xiaojuan</au><au>Gao, Hu</au><au>Li, Xihong</au><au>Qu, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Roles of Lpar1 in Central Nervous System Disorders and Diseases</atitle><jtitle>Frontiers in neuroscience</jtitle><date>2021-07-27</date><risdate>2021</risdate><volume>15</volume><spage>710473</spage><epage>710473</epage><pages>710473-710473</pages><issn>1662-453X</issn><issn>1662-4548</issn><eissn>1662-453X</eissn><abstract>Lysophosphatidic acid receptor 1 (Lpar1) , which is found in almost all human tissues but is most abundant in the brain, can couple to G protein-coupled receptors (GPCRs) and participate in regulating cell proliferation, migration, survival, and apoptosis. Endothelial differentiation gene-2 receptor (Edg2), the protein encoded by the Lpar1 gene, is present on various cell types in the central nervous system (CNS), such as neural stem cells (NSCs), oligodendrocytes, neurons, astrocytes, and microglia. Lpar1 deletion causes neurodevelopmental disorders and CNS diseases, such as brain cancer, neuropsychiatric disorders, demyelination diseases, and neuropathic pain. Here, we summarize the possible roles and mechanisms of Lpar1/ Edg2 in CNS disorders and diseases and propose that Lpar1/ Edg2 might be a potential therapeutic target for CNS disorders and diseases.</abstract><cop>Lausanne</cop><pub>Frontiers Research Foundation</pub><pmid>34385905</pmid><doi>10.3389/fnins.2021.710473</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis astrocyte Astrocytes astroglia Binding sites Biosynthesis Brain Cell cycle Cell migration Cell proliferation Cell survival Central nervous system Demyelination Edg2 Endoplasmic reticulum G protein-coupled receptors Kinases Ligands Lpar1 Lysophosphatidic acid Mental disorders Microglia Morphology Mutation Nervous system Neural stem cells Neuralgia Neurodevelopmental disorders Neurogenesis Neuroscience oligodendrocyte Oligodendrocytes Proteins Roles Stem cells Therapeutic targets |
title | The Roles of Lpar1 in Central Nervous System Disorders and Diseases |
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