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Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling
Leucine-rich glioma inactivated 1 (Lgi1), a putative tumor suppressor, is tightly associated with autosomal dominant lateral temporal lobe epilepsy (ADLTE). It has been shown that Lgi1 regulates the myelination of Schwann cells in the peripheral nervous system (PNS). However, the function and underl...
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| Published in: | Frontiers in molecular neuroscience 2018-07, Vol.11, p.231-231 |
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| container_title | Frontiers in molecular neuroscience |
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| creator | Xie, Ya-Jun Zhou, Lin Wang, Yin Jiang, Nan-Wei Cao, Shenglong Shao, Chong-Yu Wang, Xin-Tai Li, Xiang-Yao Shen, Ying Zhou, Liang |
| description | Leucine-rich glioma inactivated 1 (Lgi1), a putative tumor suppressor, is tightly associated with autosomal dominant lateral temporal lobe epilepsy (ADLTE). It has been shown that Lgi1 regulates the myelination of Schwann cells in the peripheral nervous system (PNS). However, the function and underlying mechanisms for Lgi1 regulation of oligodendrocyte differentiation and myelination in the central nervous system (CNS) remain elusive. In addition, whether Lgi1 is required for myelin maintenance is unknown. Here, we show that Lgi1 is necessary and sufficient for the differentiation of oligodendrocyte precursor cells and is also required for the maintenance of myelinated fibers. The hypomyelination in
mice attributes to the inhibition of the biosynthesis of lipids and proteins in oligodendrocytes (OLs). Moreover, we found that Lgi1 deficiency leads to a decrease in expression of tuberous sclerosis complex 1 (TSC1) and activates mammalian target of rapamycin signaling. Together, the present work establishes that Lgi1 is a regulator of oligodendrocyte development and myelination in CNS. |
| doi_str_mv | 10.3389/fnmol.2018.00231 |
| format | article |
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mice attributes to the inhibition of the biosynthesis of lipids and proteins in oligodendrocytes (OLs). Moreover, we found that Lgi1 deficiency leads to a decrease in expression of tuberous sclerosis complex 1 (TSC1) and activates mammalian target of rapamycin signaling. Together, the present work establishes that Lgi1 is a regulator of oligodendrocyte development and myelination in CNS.</description><identifier>ISSN: 1662-5099</identifier><identifier>EISSN: 1662-5099</identifier><identifier>DOI: 10.3389/fnmol.2018.00231</identifier><identifier>PMID: 30034322</identifier><language>eng</language><publisher>Switzerland: Frontiers Research Foundation</publisher><subject>Brain ; Cell differentiation ; Central nervous system ; Epilepsy ; Experiments ; Fatty acids ; Glial stem cells ; Glioma ; Glycoproteins ; Immunoglobulins ; Laboratories ; Leucine ; Lgi1 ; LGI1 protein ; Lipids ; mTOR ; Myelination ; Nervous system ; Neurobiology ; Neuroscience ; Neurosciences ; oligodendrocyte ; oligodendrocyte precursor cell ; Oligodendrocytes ; Proteins ; Rapamycin ; Schwann cells ; Temporal lobe ; TOR protein ; Tuberous sclerosis ; Tumor suppressor genes</subject><ispartof>Frontiers in molecular neuroscience, 2018-07, Vol.11, p.231-231</ispartof><rights>2018. 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 © 2018 Xie, Zhou, Wang, Jiang, Cao, Shao, Wang, Li, Shen and Zhou. 2018 Xie, Zhou, Wang, Jiang, Cao, Shao, Wang, Li, Shen and Zhou</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-d8b3c8e9c027f2ffbfe125a99e501f95f22592202ee411569c4c4a5c9e118af93</citedby><cites>FETCH-LOGICAL-c490t-d8b3c8e9c027f2ffbfe125a99e501f95f22592202ee411569c4c4a5c9e118af93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2309500477/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2309500477?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30034322$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Ya-Jun</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Wang, Yin</creatorcontrib><creatorcontrib>Jiang, Nan-Wei</creatorcontrib><creatorcontrib>Cao, Shenglong</creatorcontrib><creatorcontrib>Shao, Chong-Yu</creatorcontrib><creatorcontrib>Wang, Xin-Tai</creatorcontrib><creatorcontrib>Li, Xiang-Yao</creatorcontrib><creatorcontrib>Shen, Ying</creatorcontrib><creatorcontrib>Zhou, Liang</creatorcontrib><title>Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling</title><title>Frontiers in molecular neuroscience</title><addtitle>Front Mol Neurosci</addtitle><description>Leucine-rich glioma inactivated 1 (Lgi1), a putative tumor suppressor, is tightly associated with autosomal dominant lateral temporal lobe epilepsy (ADLTE). It has been shown that Lgi1 regulates the myelination of Schwann cells in the peripheral nervous system (PNS). However, the function and underlying mechanisms for Lgi1 regulation of oligodendrocyte differentiation and myelination in the central nervous system (CNS) remain elusive. In addition, whether Lgi1 is required for myelin maintenance is unknown. Here, we show that Lgi1 is necessary and sufficient for the differentiation of oligodendrocyte precursor cells and is also required for the maintenance of myelinated fibers. The hypomyelination in
mice attributes to the inhibition of the biosynthesis of lipids and proteins in oligodendrocytes (OLs). Moreover, we found that Lgi1 deficiency leads to a decrease in expression of tuberous sclerosis complex 1 (TSC1) and activates mammalian target of rapamycin signaling. Together, the present work establishes that Lgi1 is a regulator of oligodendrocyte development and myelination in CNS.</description><subject>Brain</subject><subject>Cell differentiation</subject><subject>Central nervous system</subject><subject>Epilepsy</subject><subject>Experiments</subject><subject>Fatty acids</subject><subject>Glial stem cells</subject><subject>Glioma</subject><subject>Glycoproteins</subject><subject>Immunoglobulins</subject><subject>Laboratories</subject><subject>Leucine</subject><subject>Lgi1</subject><subject>LGI1 protein</subject><subject>Lipids</subject><subject>mTOR</subject><subject>Myelination</subject><subject>Nervous system</subject><subject>Neurobiology</subject><subject>Neuroscience</subject><subject>Neurosciences</subject><subject>oligodendrocyte</subject><subject>oligodendrocyte precursor cell</subject><subject>Oligodendrocytes</subject><subject>Proteins</subject><subject>Rapamycin</subject><subject>Schwann cells</subject><subject>Temporal lobe</subject><subject>TOR protein</subject><subject>Tuberous sclerosis</subject><subject>Tumor suppressor genes</subject><issn>1662-5099</issn><issn>1662-5099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkk2P0zAQhiMEYj_gzglZ4sIlZWzHTnxBQoVdKhUV7Zaz5TjjrqvE3nWSSv33pO2y2uU0npl3Hs1Yb5Z9oDDjvFJfXOhiO2NAqxkA4_RVdk6lZLkApV4_e59lF32_BZBMCv42O-MAvOCMnWcPSxytD5jfeHtHrlsfO0MWwdjB78yADaHkd4pdHLAnq9ZvYoOhSdHuByTfvXOYMAzeDD4GYkJDfu2x9eGU77wh69t53q1XN-TWb4KZWpt32Rtn2h7fP8bL7M_Vj_X8Z75cXS_m35a5LRQMeVPV3FaoLLDSMedqh5QJoxQKoE4Jx5hQjAFDLCgVUtnCFkZYhZRWxil-mS1O3Caarb5PvjNpr6Px-liIaaNNGrxtUdeSlTVUxjbMFFKJmpXSFZVzEktnq3JifT2x7se6w8ZONyfTvoC-7AR_pzdxpyUUXJZsAnx-BKT4MGI_6M73FtvWBIxjrxmUBWVlReUk_fSfdBvHNP3dpOKgBEBRHjaCk8qm2PcJ3dMyFPTBG_roDX3whj56Yxr5-PyIp4F_ZuB_AawCtvo</recordid><startdate>20180706</startdate><enddate>20180706</enddate><creator>Xie, Ya-Jun</creator><creator>Zhou, Lin</creator><creator>Wang, Yin</creator><creator>Jiang, Nan-Wei</creator><creator>Cao, Shenglong</creator><creator>Shao, Chong-Yu</creator><creator>Wang, Xin-Tai</creator><creator>Li, Xiang-Yao</creator><creator>Shen, Ying</creator><creator>Zhou, Liang</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</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>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20180706</creationdate><title>Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling</title><author>Xie, Ya-Jun ; Zhou, Lin ; Wang, Yin ; Jiang, Nan-Wei ; Cao, Shenglong ; Shao, Chong-Yu ; Wang, Xin-Tai ; Li, Xiang-Yao ; Shen, Ying ; Zhou, Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-d8b3c8e9c027f2ffbfe125a99e501f95f22592202ee411569c4c4a5c9e118af93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Brain</topic><topic>Cell differentiation</topic><topic>Central nervous system</topic><topic>Epilepsy</topic><topic>Experiments</topic><topic>Fatty acids</topic><topic>Glial stem cells</topic><topic>Glioma</topic><topic>Glycoproteins</topic><topic>Immunoglobulins</topic><topic>Laboratories</topic><topic>Leucine</topic><topic>Lgi1</topic><topic>LGI1 protein</topic><topic>Lipids</topic><topic>mTOR</topic><topic>Myelination</topic><topic>Nervous system</topic><topic>Neurobiology</topic><topic>Neuroscience</topic><topic>Neurosciences</topic><topic>oligodendrocyte</topic><topic>oligodendrocyte precursor cell</topic><topic>Oligodendrocytes</topic><topic>Proteins</topic><topic>Rapamycin</topic><topic>Schwann cells</topic><topic>Temporal lobe</topic><topic>TOR protein</topic><topic>Tuberous sclerosis</topic><topic>Tumor suppressor genes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Ya-Jun</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Wang, Yin</creatorcontrib><creatorcontrib>Jiang, Nan-Wei</creatorcontrib><creatorcontrib>Cao, Shenglong</creatorcontrib><creatorcontrib>Shao, Chong-Yu</creatorcontrib><creatorcontrib>Wang, Xin-Tai</creatorcontrib><creatorcontrib>Li, Xiang-Yao</creatorcontrib><creatorcontrib>Shen, Ying</creatorcontrib><creatorcontrib>Zhou, Liang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</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 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>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 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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Ya-Jun</au><au>Zhou, Lin</au><au>Wang, Yin</au><au>Jiang, Nan-Wei</au><au>Cao, Shenglong</au><au>Shao, Chong-Yu</au><au>Wang, Xin-Tai</au><au>Li, Xiang-Yao</au><au>Shen, Ying</au><au>Zhou, Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling</atitle><jtitle>Frontiers in molecular neuroscience</jtitle><addtitle>Front Mol Neurosci</addtitle><date>2018-07-06</date><risdate>2018</risdate><volume>11</volume><spage>231</spage><epage>231</epage><pages>231-231</pages><issn>1662-5099</issn><eissn>1662-5099</eissn><abstract>Leucine-rich glioma inactivated 1 (Lgi1), a putative tumor suppressor, is tightly associated with autosomal dominant lateral temporal lobe epilepsy (ADLTE). It has been shown that Lgi1 regulates the myelination of Schwann cells in the peripheral nervous system (PNS). However, the function and underlying mechanisms for Lgi1 regulation of oligodendrocyte differentiation and myelination in the central nervous system (CNS) remain elusive. In addition, whether Lgi1 is required for myelin maintenance is unknown. Here, we show that Lgi1 is necessary and sufficient for the differentiation of oligodendrocyte precursor cells and is also required for the maintenance of myelinated fibers. The hypomyelination in
mice attributes to the inhibition of the biosynthesis of lipids and proteins in oligodendrocytes (OLs). Moreover, we found that Lgi1 deficiency leads to a decrease in expression of tuberous sclerosis complex 1 (TSC1) and activates mammalian target of rapamycin signaling. Together, the present work establishes that Lgi1 is a regulator of oligodendrocyte development and myelination in CNS.</abstract><cop>Switzerland</cop><pub>Frontiers Research Foundation</pub><pmid>30034322</pmid><doi>10.3389/fnmol.2018.00231</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Brain Cell differentiation Central nervous system Epilepsy Experiments Fatty acids Glial stem cells Glioma Glycoproteins Immunoglobulins Laboratories Leucine Lgi1 LGI1 protein Lipids mTOR Myelination Nervous system Neurobiology Neuroscience Neurosciences oligodendrocyte oligodendrocyte precursor cell Oligodendrocytes Proteins Rapamycin Schwann cells Temporal lobe TOR protein Tuberous sclerosis Tumor suppressor genes |
| title | Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling |
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