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Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum
A-kinase anchor protein 12 (AKAP12), a scaffold protein, has been implicated in the central nervous system, including blood-brain barrier (BBB) function. Although its expression level in the corpus callosum is higher than in other brain regions, such as the cerebral cortex, the role of AKAP12 in the...
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Published in: | Bioinformatics and biology insights 2024-01, Vol.18, p.11779322241276936 |
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creator | Hoshino, Tomonori Takase, Hajime Ishikawa, Hidehiro Hamanaka, Gen Kimura, Shintaro Fukuda, Norito Park, Ji Hyun Nakajima, Hiroki Shirakawa, Hisashi Shindo, Akihiro Kim, Kyu-Won H Gelman, Irwin Lok, Josephine Arai, Ken |
description | A-kinase anchor protein 12 (AKAP12), a scaffold protein, has been implicated in the central nervous system, including blood-brain barrier (BBB) function. Although its expression level in the corpus callosum is higher than in other brain regions, such as the cerebral cortex, the role of AKAP12 in the corpus callosum remains unclear. In this study, we investigate the impact of AKAP12 deficiency by transcriptome analysis using RNA-sequencing (RNA-seq) on the corpus callosum of AKAP12 knockout (KO) mice. We observed minimal changes, with only 13 genes showing differential expression, including
itself. Notably,
and
, genes potentially involved in BBB function, were downregulated in AKAP12 KO mice and expressed in vascular cells similar to
. These changes in gene expression may affect important biological pathways that may be associated with neurological disorders. Our findings provide an additional data set for future research on the role of AKAP12 in the central nervous system. |
doi_str_mv | 10.1177/11779322241276936 |
format | article |
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itself. Notably,
and
, genes potentially involved in BBB function, were downregulated in AKAP12 KO mice and expressed in vascular cells similar to
. These changes in gene expression may affect important biological pathways that may be associated with neurological disorders. Our findings provide an additional data set for future research on the role of AKAP12 in the central nervous system.</description><identifier>ISSN: 1177-9322</identifier><identifier>EISSN: 1177-9322</identifier><identifier>DOI: 10.1177/11779322241276936</identifier><identifier>PMID: 39345723</identifier><language>eng</language><publisher>United States: SAGE Publications</publisher><subject>Short Communication</subject><ispartof>Bioinformatics and biology insights, 2024-01, Vol.18, p.11779322241276936</ispartof><rights>The Author(s) 2024.</rights><rights>The Author(s) 2024 2024 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0003-1615-3258 ; 0000-0002-1548-0516</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439161/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439161/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,37013,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39345723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hoshino, Tomonori</creatorcontrib><creatorcontrib>Takase, Hajime</creatorcontrib><creatorcontrib>Ishikawa, Hidehiro</creatorcontrib><creatorcontrib>Hamanaka, Gen</creatorcontrib><creatorcontrib>Kimura, Shintaro</creatorcontrib><creatorcontrib>Fukuda, Norito</creatorcontrib><creatorcontrib>Park, Ji Hyun</creatorcontrib><creatorcontrib>Nakajima, Hiroki</creatorcontrib><creatorcontrib>Shirakawa, Hisashi</creatorcontrib><creatorcontrib>Shindo, Akihiro</creatorcontrib><creatorcontrib>Kim, Kyu-Won</creatorcontrib><creatorcontrib>H Gelman, Irwin</creatorcontrib><creatorcontrib>Lok, Josephine</creatorcontrib><creatorcontrib>Arai, Ken</creatorcontrib><title>Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum</title><title>Bioinformatics and biology insights</title><addtitle>Bioinform Biol Insights</addtitle><description>A-kinase anchor protein 12 (AKAP12), a scaffold protein, has been implicated in the central nervous system, including blood-brain barrier (BBB) function. Although its expression level in the corpus callosum is higher than in other brain regions, such as the cerebral cortex, the role of AKAP12 in the corpus callosum remains unclear. In this study, we investigate the impact of AKAP12 deficiency by transcriptome analysis using RNA-sequencing (RNA-seq) on the corpus callosum of AKAP12 knockout (KO) mice. We observed minimal changes, with only 13 genes showing differential expression, including
itself. Notably,
and
, genes potentially involved in BBB function, were downregulated in AKAP12 KO mice and expressed in vascular cells similar to
. These changes in gene expression may affect important biological pathways that may be associated with neurological disorders. Our findings provide an additional data set for future research on the role of AKAP12 in the central nervous system.</description><subject>Short Communication</subject><issn>1177-9322</issn><issn>1177-9322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkUtPwzAMxyME4jH4AFxQj1wGcdKl6QlNYzzEEBzGOcoTgtpmJC3Svj0tDMRkybb-tn62bIROAV8AFMXl4EpKCMmBFKykbAcdDtp4EHf_5QfoKKV3jBnwgu2jA1rSfFIQeojmyyibpKNftaH2OnuOwfnKpiy4bPowfQaSXVvntbeNXme-yR5Dl2w2C3HVpWwmqyqkrj5Ge05WyZ5s4gi93MyXs7vx4un2fjZdjA3FrB0zSajKLSac96sRUxLJS4W51s5hi7WinChaKiCqN-sYNxM6IWCMksoRQ0fo_odrgnwXq-hrGdciSC--hRBfhYyt15UV4EzBjCUTgDzXwKQDiZXLOUjGKR5YVz-sVadqa7Rt2iirLeh2pfFv4jV8ih5IS2DQE843hBg-OptaUfukbVXJxvZXEhQACGZ5ObSe_R_2N-X3EfQLg2eKag</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Hoshino, Tomonori</creator><creator>Takase, Hajime</creator><creator>Ishikawa, Hidehiro</creator><creator>Hamanaka, Gen</creator><creator>Kimura, Shintaro</creator><creator>Fukuda, Norito</creator><creator>Park, Ji Hyun</creator><creator>Nakajima, Hiroki</creator><creator>Shirakawa, Hisashi</creator><creator>Shindo, Akihiro</creator><creator>Kim, Kyu-Won</creator><creator>H Gelman, Irwin</creator><creator>Lok, Josephine</creator><creator>Arai, Ken</creator><general>SAGE Publications</general><general>SAGE Publishing</general><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1615-3258</orcidid><orcidid>https://orcid.org/0000-0002-1548-0516</orcidid></search><sort><creationdate>20240101</creationdate><title>Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum</title><author>Hoshino, Tomonori ; Takase, Hajime ; Ishikawa, Hidehiro ; Hamanaka, Gen ; Kimura, Shintaro ; Fukuda, Norito ; Park, Ji Hyun ; Nakajima, Hiroki ; Shirakawa, Hisashi ; Shindo, Akihiro ; Kim, Kyu-Won ; H Gelman, Irwin ; Lok, Josephine ; Arai, Ken</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-d306t-6a23b4e02881172d92a89b08ccff0e0cb382b39b12b2b2ef68d53521ddbabf2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Short Communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hoshino, Tomonori</creatorcontrib><creatorcontrib>Takase, Hajime</creatorcontrib><creatorcontrib>Ishikawa, Hidehiro</creatorcontrib><creatorcontrib>Hamanaka, Gen</creatorcontrib><creatorcontrib>Kimura, Shintaro</creatorcontrib><creatorcontrib>Fukuda, Norito</creatorcontrib><creatorcontrib>Park, Ji Hyun</creatorcontrib><creatorcontrib>Nakajima, Hiroki</creatorcontrib><creatorcontrib>Shirakawa, Hisashi</creatorcontrib><creatorcontrib>Shindo, Akihiro</creatorcontrib><creatorcontrib>Kim, Kyu-Won</creatorcontrib><creatorcontrib>H Gelman, Irwin</creatorcontrib><creatorcontrib>Lok, Josephine</creatorcontrib><creatorcontrib>Arai, Ken</creatorcontrib><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJÂ Directory of Open Access Journals</collection><jtitle>Bioinformatics and biology insights</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hoshino, Tomonori</au><au>Takase, Hajime</au><au>Ishikawa, Hidehiro</au><au>Hamanaka, Gen</au><au>Kimura, Shintaro</au><au>Fukuda, Norito</au><au>Park, Ji Hyun</au><au>Nakajima, Hiroki</au><au>Shirakawa, Hisashi</au><au>Shindo, Akihiro</au><au>Kim, Kyu-Won</au><au>H Gelman, Irwin</au><au>Lok, Josephine</au><au>Arai, Ken</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum</atitle><jtitle>Bioinformatics and biology insights</jtitle><addtitle>Bioinform Biol Insights</addtitle><date>2024-01-01</date><risdate>2024</risdate><volume>18</volume><spage>11779322241276936</spage><pages>11779322241276936-</pages><issn>1177-9322</issn><eissn>1177-9322</eissn><abstract>A-kinase anchor protein 12 (AKAP12), a scaffold protein, has been implicated in the central nervous system, including blood-brain barrier (BBB) function. Although its expression level in the corpus callosum is higher than in other brain regions, such as the cerebral cortex, the role of AKAP12 in the corpus callosum remains unclear. In this study, we investigate the impact of AKAP12 deficiency by transcriptome analysis using RNA-sequencing (RNA-seq) on the corpus callosum of AKAP12 knockout (KO) mice. We observed minimal changes, with only 13 genes showing differential expression, including
itself. Notably,
and
, genes potentially involved in BBB function, were downregulated in AKAP12 KO mice and expressed in vascular cells similar to
. These changes in gene expression may affect important biological pathways that may be associated with neurological disorders. Our findings provide an additional data set for future research on the role of AKAP12 in the central nervous system.</abstract><cop>United States</cop><pub>SAGE Publications</pub><pmid>39345723</pmid><doi>10.1177/11779322241276936</doi><orcidid>https://orcid.org/0000-0003-1615-3258</orcidid><orcidid>https://orcid.org/0000-0002-1548-0516</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Short Communication |
title | Transcriptomic Profiles of AKAP12 Deficiency in Mouse Corpus Callosum |
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