Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development
Aims Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study...
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| Veröffentlicht in: | Neuropathology and applied neurobiology 2023-04, Vol.49 (2), p.e12890-n/a |
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| creator | Huang, Chia‐Wei Lee, Kuang‐Yung Lin, Peng‐Tzu Nian, Fang‐Shin Cheng, Haw‐Yuan Chang, Chien‐Hui Liao, Cheng‐Yen Su, Yen‐Lin Seah, Carol Li, Ching Chen, Yu‐Fu Lee, Mei‐Hsuan Tsai, Jin‐Wu |
| description | Aims
Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models.
Methods
To create Mbnl2 knockout neurons, cDNA encoding Cre‐recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two‐photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis.
Results
We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2.
Conclusion
MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis‐splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis.
In Mbnl2‐knockout mouse model of myotonic dystrophy (DM), the density and dynamics of dendritic spines of cortical neurons were decreased during adolescence. Meanwhile, adducin 1 (ADD1) switched from adult to fetal isoform with a frameshift, causing the truncated ADD1 failing to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. Their roles in maintaining the dynamics and homeostasis of dendritic spines in the developing brain may underlie the neurological symptoms in DM patients. |
| doi_str_mv | 10.1111/nan.12890 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2775625761</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2805427702</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3880-9624c4af2ef60e7696988b58f7ad6b873a51652282b6eafcf6fce4bd25e2b9b83</originalsourceid><addsrcrecordid>eNp10c9uFSEUBnBibOy1uvAFDIkbXUwLzMAwy6axatLWja4n_DkovQyMMKO9Ox_B-Ig-ibS3ujCRDQt--XIOH0LPKDmm9ZxEFY8pkwN5gDa0Fbxhw0Aeog1pCW-o7MQhelzKNSGE92J4hA5b0Qveyn6Dfl6uxQTQwUf76_uP4LeAGd7GZLZpXXD57N1SsLJ2NT5iin1JLuUJw82coRSfIlbRYhUWyAVbiDb7xRtcZh8B211UkzcFJ4dNyvVBBRxhzSlWvGYfP2GdVU228BVCmieIyxN04FQo8PT-PkIfz19_OHvbXLx_8-7s9KIxrZSkGQTrTKccAycI1L3EIKXm0vXKCi37VnEqOGOSaQHKGSecgU5bxoHpQcv2CL3c5845fVmhLOPki4EQVIS0lpH1PRes_hit9MU_9DqtOdbpRiYJ7yolrKpXe2VyKiWDG-fsJ5V3IyXjbVFjLWq8K6ra5_eJq57A_pV_mqngZA---QC7_yeNV6dX-8jfGy-gnQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2805427702</pqid></control><display><type>article</type><title>Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Huang, Chia‐Wei ; Lee, Kuang‐Yung ; Lin, Peng‐Tzu ; Nian, Fang‐Shin ; Cheng, Haw‐Yuan ; Chang, Chien‐Hui ; Liao, Cheng‐Yen ; Su, Yen‐Lin ; Seah, Carol ; Li, Ching ; Chen, Yu‐Fu ; Lee, Mei‐Hsuan ; Tsai, Jin‐Wu</creator><creatorcontrib>Huang, Chia‐Wei ; Lee, Kuang‐Yung ; Lin, Peng‐Tzu ; Nian, Fang‐Shin ; Cheng, Haw‐Yuan ; Chang, Chien‐Hui ; Liao, Cheng‐Yen ; Su, Yen‐Lin ; Seah, Carol ; Li, Ching ; Chen, Yu‐Fu ; Lee, Mei‐Hsuan ; Tsai, Jin‐Wu</creatorcontrib><description>Aims
Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models.
Methods
To create Mbnl2 knockout neurons, cDNA encoding Cre‐recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two‐photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis.
Results
We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2.
Conclusion
MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis‐splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis.
In Mbnl2‐knockout mouse model of myotonic dystrophy (DM), the density and dynamics of dendritic spines of cortical neurons were decreased during adolescence. Meanwhile, adducin 1 (ADD1) switched from adult to fetal isoform with a frameshift, causing the truncated ADD1 failing to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. Their roles in maintaining the dynamics and homeostasis of dendritic spines in the developing brain may underlie the neurological symptoms in DM patients.</description><identifier>ISSN: 0305-1846</identifier><identifier>EISSN: 1365-2990</identifier><identifier>DOI: 10.1111/nan.12890</identifier><identifier>PMID: 36765387</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Add1 ; Adducin ; Alternative splicing ; Animal models ; Animals ; Brain ; Brain - pathology ; Brain slice preparation ; dendritic spine ; Dendritic spines ; Dendritic Spines - metabolism ; Dendritic Spines - pathology ; Electroporation ; Fetuses ; Homeostasis ; Mice ; muscleblind‐like ; Myotonic dystrophy ; Myotonic Dystrophy - genetics ; Neonates ; neural development ; Neural stem cells ; Neuropathogenesis ; Phenotypes ; Protein Isoforms - metabolism ; Recombinase ; Spectrin</subject><ispartof>Neuropathology and applied neurobiology, 2023-04, Vol.49 (2), p.e12890-n/a</ispartof><rights>2023 The Authors. published by John Wiley & Sons Ltd on behalf of British Neuropathological Society.</rights><rights>2023 The Authors. Neuropathology and Applied Neurobiology published by John Wiley & Sons Ltd on behalf of British Neuropathological Society.</rights><rights>2023. This article is published 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3880-9624c4af2ef60e7696988b58f7ad6b873a51652282b6eafcf6fce4bd25e2b9b83</citedby><cites>FETCH-LOGICAL-c3880-9624c4af2ef60e7696988b58f7ad6b873a51652282b6eafcf6fce4bd25e2b9b83</cites><orcidid>0000-0003-0135-759X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnan.12890$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnan.12890$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36765387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Chia‐Wei</creatorcontrib><creatorcontrib>Lee, Kuang‐Yung</creatorcontrib><creatorcontrib>Lin, Peng‐Tzu</creatorcontrib><creatorcontrib>Nian, Fang‐Shin</creatorcontrib><creatorcontrib>Cheng, Haw‐Yuan</creatorcontrib><creatorcontrib>Chang, Chien‐Hui</creatorcontrib><creatorcontrib>Liao, Cheng‐Yen</creatorcontrib><creatorcontrib>Su, Yen‐Lin</creatorcontrib><creatorcontrib>Seah, Carol</creatorcontrib><creatorcontrib>Li, Ching</creatorcontrib><creatorcontrib>Chen, Yu‐Fu</creatorcontrib><creatorcontrib>Lee, Mei‐Hsuan</creatorcontrib><creatorcontrib>Tsai, Jin‐Wu</creatorcontrib><title>Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development</title><title>Neuropathology and applied neurobiology</title><addtitle>Neuropathol Appl Neurobiol</addtitle><description>Aims
Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models.
Methods
To create Mbnl2 knockout neurons, cDNA encoding Cre‐recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two‐photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis.
Results
We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2.
Conclusion
MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis‐splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis.
In Mbnl2‐knockout mouse model of myotonic dystrophy (DM), the density and dynamics of dendritic spines of cortical neurons were decreased during adolescence. Meanwhile, adducin 1 (ADD1) switched from adult to fetal isoform with a frameshift, causing the truncated ADD1 failing to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. Their roles in maintaining the dynamics and homeostasis of dendritic spines in the developing brain may underlie the neurological symptoms in DM patients.</description><subject>Add1</subject><subject>Adducin</subject><subject>Alternative splicing</subject><subject>Animal models</subject><subject>Animals</subject><subject>Brain</subject><subject>Brain - pathology</subject><subject>Brain slice preparation</subject><subject>dendritic spine</subject><subject>Dendritic spines</subject><subject>Dendritic Spines - metabolism</subject><subject>Dendritic Spines - pathology</subject><subject>Electroporation</subject><subject>Fetuses</subject><subject>Homeostasis</subject><subject>Mice</subject><subject>muscleblind‐like</subject><subject>Myotonic dystrophy</subject><subject>Myotonic Dystrophy - genetics</subject><subject>Neonates</subject><subject>neural development</subject><subject>Neural stem cells</subject><subject>Neuropathogenesis</subject><subject>Phenotypes</subject><subject>Protein Isoforms - metabolism</subject><subject>Recombinase</subject><subject>Spectrin</subject><issn>0305-1846</issn><issn>1365-2990</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp10c9uFSEUBnBibOy1uvAFDIkbXUwLzMAwy6axatLWja4n_DkovQyMMKO9Ox_B-Ig-ibS3ujCRDQt--XIOH0LPKDmm9ZxEFY8pkwN5gDa0Fbxhw0Aeog1pCW-o7MQhelzKNSGE92J4hA5b0Qveyn6Dfl6uxQTQwUf76_uP4LeAGd7GZLZpXXD57N1SsLJ2NT5iin1JLuUJw82coRSfIlbRYhUWyAVbiDb7xRtcZh8B211UkzcFJ4dNyvVBBRxhzSlWvGYfP2GdVU228BVCmieIyxN04FQo8PT-PkIfz19_OHvbXLx_8-7s9KIxrZSkGQTrTKccAycI1L3EIKXm0vXKCi37VnEqOGOSaQHKGSecgU5bxoHpQcv2CL3c5845fVmhLOPki4EQVIS0lpH1PRes_hit9MU_9DqtOdbpRiYJ7yolrKpXe2VyKiWDG-fsJ5V3IyXjbVFjLWq8K6ra5_eJq57A_pV_mqngZA---QC7_yeNV6dX-8jfGy-gnQ</recordid><startdate>202304</startdate><enddate>202304</enddate><creator>Huang, Chia‐Wei</creator><creator>Lee, Kuang‐Yung</creator><creator>Lin, Peng‐Tzu</creator><creator>Nian, Fang‐Shin</creator><creator>Cheng, Haw‐Yuan</creator><creator>Chang, Chien‐Hui</creator><creator>Liao, Cheng‐Yen</creator><creator>Su, Yen‐Lin</creator><creator>Seah, Carol</creator><creator>Li, Ching</creator><creator>Chen, Yu‐Fu</creator><creator>Lee, Mei‐Hsuan</creator><creator>Tsai, Jin‐Wu</creator><general>Wiley Subscription Services, Inc</general><scope>24P</scope><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>7TK</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0135-759X</orcidid></search><sort><creationdate>202304</creationdate><title>Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development</title><author>Huang, Chia‐Wei ; Lee, Kuang‐Yung ; Lin, Peng‐Tzu ; Nian, Fang‐Shin ; Cheng, Haw‐Yuan ; Chang, Chien‐Hui ; Liao, Cheng‐Yen ; Su, Yen‐Lin ; Seah, Carol ; Li, Ching ; Chen, Yu‐Fu ; Lee, Mei‐Hsuan ; Tsai, Jin‐Wu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3880-9624c4af2ef60e7696988b58f7ad6b873a51652282b6eafcf6fce4bd25e2b9b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Add1</topic><topic>Adducin</topic><topic>Alternative splicing</topic><topic>Animal models</topic><topic>Animals</topic><topic>Brain</topic><topic>Brain - pathology</topic><topic>Brain slice preparation</topic><topic>dendritic spine</topic><topic>Dendritic spines</topic><topic>Dendritic Spines - metabolism</topic><topic>Dendritic Spines - pathology</topic><topic>Electroporation</topic><topic>Fetuses</topic><topic>Homeostasis</topic><topic>Mice</topic><topic>muscleblind‐like</topic><topic>Myotonic dystrophy</topic><topic>Myotonic Dystrophy - genetics</topic><topic>Neonates</topic><topic>neural development</topic><topic>Neural stem cells</topic><topic>Neuropathogenesis</topic><topic>Phenotypes</topic><topic>Protein Isoforms - metabolism</topic><topic>Recombinase</topic><topic>Spectrin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Chia‐Wei</creatorcontrib><creatorcontrib>Lee, Kuang‐Yung</creatorcontrib><creatorcontrib>Lin, Peng‐Tzu</creatorcontrib><creatorcontrib>Nian, Fang‐Shin</creatorcontrib><creatorcontrib>Cheng, Haw‐Yuan</creatorcontrib><creatorcontrib>Chang, Chien‐Hui</creatorcontrib><creatorcontrib>Liao, Cheng‐Yen</creatorcontrib><creatorcontrib>Su, Yen‐Lin</creatorcontrib><creatorcontrib>Seah, Carol</creatorcontrib><creatorcontrib>Li, Ching</creatorcontrib><creatorcontrib>Chen, Yu‐Fu</creatorcontrib><creatorcontrib>Lee, Mei‐Hsuan</creatorcontrib><creatorcontrib>Tsai, Jin‐Wu</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropathology and applied neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Chia‐Wei</au><au>Lee, Kuang‐Yung</au><au>Lin, Peng‐Tzu</au><au>Nian, Fang‐Shin</au><au>Cheng, Haw‐Yuan</au><au>Chang, Chien‐Hui</au><au>Liao, Cheng‐Yen</au><au>Su, Yen‐Lin</au><au>Seah, Carol</au><au>Li, Ching</au><au>Chen, Yu‐Fu</au><au>Lee, Mei‐Hsuan</au><au>Tsai, Jin‐Wu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development</atitle><jtitle>Neuropathology and applied neurobiology</jtitle><addtitle>Neuropathol Appl Neurobiol</addtitle><date>2023-04</date><risdate>2023</risdate><volume>49</volume><issue>2</issue><spage>e12890</spage><epage>n/a</epage><pages>e12890-n/a</pages><issn>0305-1846</issn><eissn>1365-2990</eissn><abstract>Aims
Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models.
Methods
To create Mbnl2 knockout neurons, cDNA encoding Cre‐recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two‐photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis.
Results
We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2.
Conclusion
MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis‐splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis.
In Mbnl2‐knockout mouse model of myotonic dystrophy (DM), the density and dynamics of dendritic spines of cortical neurons were decreased during adolescence. Meanwhile, adducin 1 (ADD1) switched from adult to fetal isoform with a frameshift, causing the truncated ADD1 failing to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. Their roles in maintaining the dynamics and homeostasis of dendritic spines in the developing brain may underlie the neurological symptoms in DM patients.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>36765387</pmid><doi>10.1111/nan.12890</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0003-0135-759X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Add1 Adducin Alternative splicing Animal models Animals Brain Brain - pathology Brain slice preparation dendritic spine Dendritic spines Dendritic Spines - metabolism Dendritic Spines - pathology Electroporation Fetuses Homeostasis Mice muscleblind‐like Myotonic dystrophy Myotonic Dystrophy - genetics Neonates neural development Neural stem cells Neuropathogenesis Phenotypes Protein Isoforms - metabolism Recombinase Spectrin |
| title | Muscleblind‐like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development |
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