A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation
Refsum disease (RfD) is an autosomal recessive neurologic disorder of the lipid metabolism. We have identified a novel murine long-chain acyl-CoA synthetase (mLACS) associated with the RfD gene using yeast two-hybrid assay. Northern blot analyses revealed that mLACS was expressed mainly in the brain...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2003-06, Vol.305 (4), p.925-933 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Kee, Hae Jin Koh, Jeong Tae Yang, Sung Yeul Lee, Zang Hee Baik, Yung Hong Kim, Kyung Keun |
| description | Refsum disease (RfD) is an autosomal recessive neurologic disorder of the lipid metabolism. We have identified a novel murine long-chain acyl-CoA synthetase (mLACS) associated with the RfD gene using yeast two-hybrid assay. Northern blot analyses revealed that
mLACS was expressed mainly in the brain and testis.
mLACS was highly expressed in the brain at 2 weeks after birth and maintained through adult life. Expressions of the brain-specific
LACS family increased in the PC12 cells undergoing neurite outgrowth by nerve growth factor. mLACS preferentially catalyzed the formation of arachidonoyl-CoA more than palmitoyl-CoA or oleoyl-CoA in PC12 cells. Triacsin C, an inhibitor of LACS, suppressed the cell proliferation and decreased mLACS expression in parent PC12 cells, but not in stably anti-sense mLACS cDNA-transfected cells. Our results indicate that mLACS participates in neuronal cell proliferation and differentiation, and interaction of the RfD gene with brain-selective mLACS may be involved in the pathogenesis of RfD. |
| doi_str_mv | 10.1016/S0006-291X(03)00859-3 |
| format | Article |
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mLACS was expressed mainly in the brain and testis.
mLACS was highly expressed in the brain at 2 weeks after birth and maintained through adult life. Expressions of the brain-specific
LACS family increased in the PC12 cells undergoing neurite outgrowth by nerve growth factor. mLACS preferentially catalyzed the formation of arachidonoyl-CoA more than palmitoyl-CoA or oleoyl-CoA in PC12 cells. Triacsin C, an inhibitor of LACS, suppressed the cell proliferation and decreased mLACS expression in parent PC12 cells, but not in stably anti-sense mLACS cDNA-transfected cells. Our results indicate that mLACS participates in neuronal cell proliferation and differentiation, and interaction of the RfD gene with brain-selective mLACS may be involved in the pathogenesis of RfD.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/S0006-291X(03)00859-3</identifier><identifier>PMID: 12767919</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Sequence ; Animals ; Brain - enzymology ; Brain-specific ; Cell Division ; Cell Line ; Cell Survival ; Cloning, Molecular ; Coenzyme A Ligases - genetics ; Coenzyme A Ligases - metabolism ; Coenzyme A Ligases - physiology ; Enzyme Inhibitors - pharmacology ; Long-chain acyl-CoA synthetase ; Mice ; Mixed Function Oxygenases - metabolism ; Molecular Sequence Data ; Nerve Growth Factor - pharmacology ; Neurons - enzymology ; PC12 Cells ; Phytanoyl-CoA α-hydroxylase ; Rats ; Refsum disease ; Repressor Proteins ; Saccharomyces cerevisiae Proteins ; Sequence Alignment ; Tissue Distribution ; Transcription, Genetic ; Triacsin C ; Triazenes - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2003-06, Vol.305 (4), p.925-933</ispartof><rights>2003 Elsevier Science (USA)</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c458t-e7d2d526c4ad33ab41bf8b07db15117f380426d699629e7a1d6d52fe892db0793</citedby><cites>FETCH-LOGICAL-c458t-e7d2d526c4ad33ab41bf8b07db15117f380426d699629e7a1d6d52fe892db0793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-291X(03)00859-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12767919$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kee, Hae Jin</creatorcontrib><creatorcontrib>Koh, Jeong Tae</creatorcontrib><creatorcontrib>Yang, Sung Yeul</creatorcontrib><creatorcontrib>Lee, Zang Hee</creatorcontrib><creatorcontrib>Baik, Yung Hong</creatorcontrib><creatorcontrib>Kim, Kyung Keun</creatorcontrib><title>A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Refsum disease (RfD) is an autosomal recessive neurologic disorder of the lipid metabolism. We have identified a novel murine long-chain acyl-CoA synthetase (mLACS) associated with the RfD gene using yeast two-hybrid assay. Northern blot analyses revealed that
mLACS was expressed mainly in the brain and testis.
mLACS was highly expressed in the brain at 2 weeks after birth and maintained through adult life. Expressions of the brain-specific
LACS family increased in the PC12 cells undergoing neurite outgrowth by nerve growth factor. mLACS preferentially catalyzed the formation of arachidonoyl-CoA more than palmitoyl-CoA or oleoyl-CoA in PC12 cells. Triacsin C, an inhibitor of LACS, suppressed the cell proliferation and decreased mLACS expression in parent PC12 cells, but not in stably anti-sense mLACS cDNA-transfected cells. Our results indicate that mLACS participates in neuronal cell proliferation and differentiation, and interaction of the RfD gene with brain-selective mLACS may be involved in the pathogenesis of RfD.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Brain - enzymology</subject><subject>Brain-specific</subject><subject>Cell Division</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Cloning, Molecular</subject><subject>Coenzyme A Ligases - genetics</subject><subject>Coenzyme A Ligases - metabolism</subject><subject>Coenzyme A Ligases - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Long-chain acyl-CoA synthetase</subject><subject>Mice</subject><subject>Mixed Function Oxygenases - metabolism</subject><subject>Molecular Sequence Data</subject><subject>Nerve Growth Factor - pharmacology</subject><subject>Neurons - enzymology</subject><subject>PC12 Cells</subject><subject>Phytanoyl-CoA α-hydroxylase</subject><subject>Rats</subject><subject>Refsum disease</subject><subject>Repressor Proteins</subject><subject>Saccharomyces cerevisiae Proteins</subject><subject>Sequence Alignment</subject><subject>Tissue Distribution</subject><subject>Transcription, Genetic</subject><subject>Triacsin C</subject><subject>Triazenes - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1u1DAUBWALUdFp4RFAXiG6SLm2EydeodGIn0qVugAkdpZj31Ajjx3spGLenqQzgmVXlqzv-lj3EPKawTUDJt9_BQBZccV-vANxBdA1qhLPyIaBgoozqJ-TzT9yTi5K-QXAWC3VC3LOeCtbxdSGhC2N6QED3c_ZR6QhxZ-VvTc-UmMPodqlLS2HON3jZApS_DNmLAUdXUCfVzaaPHnrRzNhWW8jzjlFE6jFEOiYU_ADZjP5FF-Ss8GEgq9O5yX5_unjt92X6vbu881ue1vZuummClvHXcOlrY0TwvQ164euh9b1rGGsHUQHNZdOKiW5wtYwJxc-YKe4W5gSl-Tt8d0l_feMZdJ7X9bvmIhpLroVvOOq5k9C1rWdBA4LbI7Q5lRKxkGP2e9NPmgGeu1DP_ah12VrEPqxDy2WuTengLnfo_s_dSpgAR-OAJd9PHjMuliP0aLzGe2kXfJPRPwFaGObwQ</recordid><startdate>20030613</startdate><enddate>20030613</enddate><creator>Kee, Hae Jin</creator><creator>Koh, Jeong Tae</creator><creator>Yang, Sung Yeul</creator><creator>Lee, Zang Hee</creator><creator>Baik, Yung Hong</creator><creator>Kim, Kyung Keun</creator><general>Elsevier Inc</general><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030613</creationdate><title>A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation</title><author>Kee, Hae Jin ; Koh, Jeong Tae ; Yang, Sung Yeul ; Lee, Zang Hee ; Baik, Yung Hong ; Kim, Kyung Keun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c458t-e7d2d526c4ad33ab41bf8b07db15117f380426d699629e7a1d6d52fe892db0793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Brain - enzymology</topic><topic>Brain-specific</topic><topic>Cell Division</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Cloning, Molecular</topic><topic>Coenzyme A Ligases - genetics</topic><topic>Coenzyme A Ligases - metabolism</topic><topic>Coenzyme A Ligases - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Long-chain acyl-CoA synthetase</topic><topic>Mice</topic><topic>Mixed Function Oxygenases - metabolism</topic><topic>Molecular Sequence Data</topic><topic>Nerve Growth Factor - pharmacology</topic><topic>Neurons - enzymology</topic><topic>PC12 Cells</topic><topic>Phytanoyl-CoA α-hydroxylase</topic><topic>Rats</topic><topic>Refsum disease</topic><topic>Repressor Proteins</topic><topic>Saccharomyces cerevisiae Proteins</topic><topic>Sequence Alignment</topic><topic>Tissue Distribution</topic><topic>Transcription, Genetic</topic><topic>Triacsin C</topic><topic>Triazenes - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kee, Hae Jin</creatorcontrib><creatorcontrib>Koh, Jeong Tae</creatorcontrib><creatorcontrib>Yang, Sung Yeul</creatorcontrib><creatorcontrib>Lee, Zang Hee</creatorcontrib><creatorcontrib>Baik, Yung Hong</creatorcontrib><creatorcontrib>Kim, Kyung Keun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kee, Hae Jin</au><au>Koh, Jeong Tae</au><au>Yang, Sung Yeul</au><au>Lee, Zang Hee</au><au>Baik, Yung Hong</au><au>Kim, Kyung Keun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003-06-13</date><risdate>2003</risdate><volume>305</volume><issue>4</issue><spage>925</spage><epage>933</epage><pages>925-933</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Refsum disease (RfD) is an autosomal recessive neurologic disorder of the lipid metabolism. We have identified a novel murine long-chain acyl-CoA synthetase (mLACS) associated with the RfD gene using yeast two-hybrid assay. Northern blot analyses revealed that
mLACS was expressed mainly in the brain and testis.
mLACS was highly expressed in the brain at 2 weeks after birth and maintained through adult life. Expressions of the brain-specific
LACS family increased in the PC12 cells undergoing neurite outgrowth by nerve growth factor. mLACS preferentially catalyzed the formation of arachidonoyl-CoA more than palmitoyl-CoA or oleoyl-CoA in PC12 cells. Triacsin C, an inhibitor of LACS, suppressed the cell proliferation and decreased mLACS expression in parent PC12 cells, but not in stably anti-sense mLACS cDNA-transfected cells. Our results indicate that mLACS participates in neuronal cell proliferation and differentiation, and interaction of the RfD gene with brain-selective mLACS may be involved in the pathogenesis of RfD.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12767919</pmid><doi>10.1016/S0006-291X(03)00859-3</doi><tpages>9</tpages></addata></record> |
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| subjects | Amino Acid Sequence Animals Brain - enzymology Brain-specific Cell Division Cell Line Cell Survival Cloning, Molecular Coenzyme A Ligases - genetics Coenzyme A Ligases - metabolism Coenzyme A Ligases - physiology Enzyme Inhibitors - pharmacology Long-chain acyl-CoA synthetase Mice Mixed Function Oxygenases - metabolism Molecular Sequence Data Nerve Growth Factor - pharmacology Neurons - enzymology PC12 Cells Phytanoyl-CoA α-hydroxylase Rats Refsum disease Repressor Proteins Saccharomyces cerevisiae Proteins Sequence Alignment Tissue Distribution Transcription, Genetic Triacsin C Triazenes - pharmacology |
| title | A novel murine long-chain acyl-CoA synthetase expressed in brain participates in neuronal cell proliferation |
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