Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells
As members of the proneural basic-helix-loop-helix (bHLH) family of transcription factors, Ascl1 and Neurog2 direct the differentiation of specific populations of neurons at various times and locations within the developing nervous system. In order to characterize the mechanisms employed by these tw...
Gespeichert in:
| Veröffentlicht in: | Journal of molecular neuroscience 2015-03, Vol.55 (3), p.684-705 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 705 |
|---|---|
| container_issue | 3 |
| container_start_page | 684 |
| container_title | Journal of molecular neuroscience |
| container_volume | 55 |
| creator | Huang, Holly S. Redmond, Tanya M. Kubish, Ginger M. Gupta, Shweta Thompson, Robert C. Turner, David L. Uhler, Michael D. |
| description | As members of the proneural basic-helix-loop-helix (bHLH) family of transcription factors, Ascl1 and Neurog2 direct the differentiation of specific populations of neurons at various times and locations within the developing nervous system. In order to characterize the mechanisms employed by these two bHLH factors, we generated stable, doxycycline-inducible lines of P19 embryonic carcinoma cells that express comparable levels of
Ascl1
and
Neurog2
. Upon induction, both Ascl1 and Neurog2 directed morphological and immunocytochemical changes consistent with initiation of neuronal differentiation. Comparison of Ascl1- and Neurog2-regulated genes by microarray analyses showed both shared and distinct transcriptional changes for each bHLH protein. In both Ascl1- and Neurog2-differentiating cells, repression of Oct4 mRNA levels was accompanied by increased Oct4 promoter methylation. However, DNA demethylation was not detected for genes induced by either bHLH protein. Neurog2-induced genes included glutamatergic marker genes while Ascl1-induced genes included GABAergic marker genes. The Neurog2-specific induction of a gene encoding a protein phosphatase inhibitor,
Ppp1r14a
, was dependent on distinct, canonical E-box sequences within the
Ppp1r14a
promoter and the nucleotide sequences within these E-boxes were partially responsible for Neurog2-specific regulation. Our results illustrate multiple novel mechanisms by which Ascl1 and Neurog2 regulate gene repression during neuronal differentiation in P19 cells. |
| doi_str_mv | 10.1007/s12031-014-0408-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1660387919</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3579731361</sourcerecordid><originalsourceid>FETCH-LOGICAL-c471t-526e6cc36c6623018cee67d36bd6ab1fff9d1a56aa077e8f4e4e4d9ec2572d6c3</originalsourceid><addsrcrecordid>eNqNkUFrFDEYhoNY7Lr6A7xIwEsvY_NlJpnkWLZbLRQVqeeQySRLykyyJjPCHv3nZpwqIgiSQwg875uP70HoFZC3QEh7mYGSGioCTUUaIir6BG2AMVkBcP4UbYiQrBJc8nP0POcHQig0IJ6hc8pAyBrEBn2_Tzpkk_xx8jHoAX-2h3nQU0wnvP9mw5TxbfCT15PtcXfCV9kMgHXo8Qc7p3ig-HpOPhzW51Jw7Z2zqSRLplTi6PAnkHg_dukUgzd4p5PxIY4a7-ww5BfozOkh25eP9xZ9udnf795Xdx_f3e6u7irTtDBVjHLLjam54ZzWBISxlrd9zbue6w6cc7IHzbjWpG2tcI0tp5fWUNbSnpt6iy7W3mOKX2ebJzX6bMoEOtg4Z1VWRmrRSpD_gTLaMCJLYIve_IU-xDmVPfykoAZJxELBSpkUc07WqWPyo04nBUQtKtWqUhWValGpaMm8fmyeu9H2vxO_3BWArkA-LgZs-uPrf7b-AIh7qXA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1651319080</pqid></control><display><type>article</type><title>Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Huang, Holly S. ; Redmond, Tanya M. ; Kubish, Ginger M. ; Gupta, Shweta ; Thompson, Robert C. ; Turner, David L. ; Uhler, Michael D.</creator><creatorcontrib>Huang, Holly S. ; Redmond, Tanya M. ; Kubish, Ginger M. ; Gupta, Shweta ; Thompson, Robert C. ; Turner, David L. ; Uhler, Michael D.</creatorcontrib><description>As members of the proneural basic-helix-loop-helix (bHLH) family of transcription factors, Ascl1 and Neurog2 direct the differentiation of specific populations of neurons at various times and locations within the developing nervous system. In order to characterize the mechanisms employed by these two bHLH factors, we generated stable, doxycycline-inducible lines of P19 embryonic carcinoma cells that express comparable levels of
Ascl1
and
Neurog2
. Upon induction, both Ascl1 and Neurog2 directed morphological and immunocytochemical changes consistent with initiation of neuronal differentiation. Comparison of Ascl1- and Neurog2-regulated genes by microarray analyses showed both shared and distinct transcriptional changes for each bHLH protein. In both Ascl1- and Neurog2-differentiating cells, repression of Oct4 mRNA levels was accompanied by increased Oct4 promoter methylation. However, DNA demethylation was not detected for genes induced by either bHLH protein. Neurog2-induced genes included glutamatergic marker genes while Ascl1-induced genes included GABAergic marker genes. The Neurog2-specific induction of a gene encoding a protein phosphatase inhibitor,
Ppp1r14a
, was dependent on distinct, canonical E-box sequences within the
Ppp1r14a
promoter and the nucleotide sequences within these E-boxes were partially responsible for Neurog2-specific regulation. Our results illustrate multiple novel mechanisms by which Ascl1 and Neurog2 regulate gene repression during neuronal differentiation in P19 cells.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-014-0408-2</identifier><identifier>PMID: 25189318</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Cell Biology ; Cell Line, Tumor ; DNA methylation ; Embryonal Carcinoma Stem Cells - cytology ; Embryonal Carcinoma Stem Cells - metabolism ; Gene Expression Regulation, Developmental ; Genes ; Kinases ; Mice ; Muscle Proteins - genetics ; Muscle Proteins - metabolism ; Nerve Tissue Proteins - metabolism ; Nervous system ; Neurochemistry ; Neurogenesis ; Neurology ; Neurons ; Neurons - cytology ; Neurons - metabolism ; Neurosciences ; Octamer Transcription Factor-3 - metabolism ; Phosphatase ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Promoter Regions, Genetic ; Proteins ; Proteomics ; Transcription factors ; Transcription, Genetic</subject><ispartof>Journal of molecular neuroscience, 2015-03, Vol.55 (3), p.684-705</ispartof><rights>Springer Science+Business Media New York 2014</rights><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-526e6cc36c6623018cee67d36bd6ab1fff9d1a56aa077e8f4e4e4d9ec2572d6c3</citedby><cites>FETCH-LOGICAL-c471t-526e6cc36c6623018cee67d36bd6ab1fff9d1a56aa077e8f4e4e4d9ec2572d6c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-014-0408-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-014-0408-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25189318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Holly S.</creatorcontrib><creatorcontrib>Redmond, Tanya M.</creatorcontrib><creatorcontrib>Kubish, Ginger M.</creatorcontrib><creatorcontrib>Gupta, Shweta</creatorcontrib><creatorcontrib>Thompson, Robert C.</creatorcontrib><creatorcontrib>Turner, David L.</creatorcontrib><creatorcontrib>Uhler, Michael D.</creatorcontrib><title>Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>As members of the proneural basic-helix-loop-helix (bHLH) family of transcription factors, Ascl1 and Neurog2 direct the differentiation of specific populations of neurons at various times and locations within the developing nervous system. In order to characterize the mechanisms employed by these two bHLH factors, we generated stable, doxycycline-inducible lines of P19 embryonic carcinoma cells that express comparable levels of
Ascl1
and
Neurog2
. Upon induction, both Ascl1 and Neurog2 directed morphological and immunocytochemical changes consistent with initiation of neuronal differentiation. Comparison of Ascl1- and Neurog2-regulated genes by microarray analyses showed both shared and distinct transcriptional changes for each bHLH protein. In both Ascl1- and Neurog2-differentiating cells, repression of Oct4 mRNA levels was accompanied by increased Oct4 promoter methylation. However, DNA demethylation was not detected for genes induced by either bHLH protein. Neurog2-induced genes included glutamatergic marker genes while Ascl1-induced genes included GABAergic marker genes. The Neurog2-specific induction of a gene encoding a protein phosphatase inhibitor,
Ppp1r14a
, was dependent on distinct, canonical E-box sequences within the
Ppp1r14a
promoter and the nucleotide sequences within these E-boxes were partially responsible for Neurog2-specific regulation. Our results illustrate multiple novel mechanisms by which Ascl1 and Neurog2 regulate gene repression during neuronal differentiation in P19 cells.</description><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>DNA methylation</subject><subject>Embryonal Carcinoma Stem Cells - cytology</subject><subject>Embryonal Carcinoma Stem Cells - metabolism</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Genes</subject><subject>Kinases</subject><subject>Mice</subject><subject>Muscle Proteins - genetics</subject><subject>Muscle Proteins - metabolism</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system</subject><subject>Neurochemistry</subject><subject>Neurogenesis</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Octamer Transcription Factor-3 - metabolism</subject><subject>Phosphatase</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Transcription factors</subject><subject>Transcription, Genetic</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkUFrFDEYhoNY7Lr6A7xIwEsvY_NlJpnkWLZbLRQVqeeQySRLykyyJjPCHv3nZpwqIgiSQwg875uP70HoFZC3QEh7mYGSGioCTUUaIir6BG2AMVkBcP4UbYiQrBJc8nP0POcHQig0IJ6hc8pAyBrEBn2_Tzpkk_xx8jHoAX-2h3nQU0wnvP9mw5TxbfCT15PtcXfCV9kMgHXo8Qc7p3ig-HpOPhzW51Jw7Z2zqSRLplTi6PAnkHg_dukUgzd4p5PxIY4a7-ww5BfozOkh25eP9xZ9udnf795Xdx_f3e6u7irTtDBVjHLLjam54ZzWBISxlrd9zbue6w6cc7IHzbjWpG2tcI0tp5fWUNbSnpt6iy7W3mOKX2ebJzX6bMoEOtg4Z1VWRmrRSpD_gTLaMCJLYIve_IU-xDmVPfykoAZJxELBSpkUc07WqWPyo04nBUQtKtWqUhWValGpaMm8fmyeu9H2vxO_3BWArkA-LgZs-uPrf7b-AIh7qXA</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Huang, Holly S.</creator><creator>Redmond, Tanya M.</creator><creator>Kubish, Ginger M.</creator><creator>Gupta, Shweta</creator><creator>Thompson, Robert C.</creator><creator>Turner, David L.</creator><creator>Uhler, Michael D.</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20150301</creationdate><title>Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells</title><author>Huang, Holly S. ; Redmond, Tanya M. ; Kubish, Ginger M. ; Gupta, Shweta ; Thompson, Robert C. ; Turner, David L. ; Uhler, Michael D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-526e6cc36c6623018cee67d36bd6ab1fff9d1a56aa077e8f4e4e4d9ec2572d6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>DNA methylation</topic><topic>Embryonal Carcinoma Stem Cells - cytology</topic><topic>Embryonal Carcinoma Stem Cells - metabolism</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Genes</topic><topic>Kinases</topic><topic>Mice</topic><topic>Muscle Proteins - genetics</topic><topic>Muscle Proteins - metabolism</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nervous system</topic><topic>Neurochemistry</topic><topic>Neurogenesis</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Octamer Transcription Factor-3 - metabolism</topic><topic>Phosphatase</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Transcription factors</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Holly S.</creatorcontrib><creatorcontrib>Redmond, Tanya M.</creatorcontrib><creatorcontrib>Kubish, Ginger M.</creatorcontrib><creatorcontrib>Gupta, Shweta</creatorcontrib><creatorcontrib>Thompson, Robert C.</creatorcontrib><creatorcontrib>Turner, David L.</creatorcontrib><creatorcontrib>Uhler, Michael D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</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>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Holly S.</au><au>Redmond, Tanya M.</au><au>Kubish, Ginger M.</au><au>Gupta, Shweta</au><au>Thompson, Robert C.</au><au>Turner, David L.</au><au>Uhler, Michael D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>55</volume><issue>3</issue><spage>684</spage><epage>705</epage><pages>684-705</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>As members of the proneural basic-helix-loop-helix (bHLH) family of transcription factors, Ascl1 and Neurog2 direct the differentiation of specific populations of neurons at various times and locations within the developing nervous system. In order to characterize the mechanisms employed by these two bHLH factors, we generated stable, doxycycline-inducible lines of P19 embryonic carcinoma cells that express comparable levels of
Ascl1
and
Neurog2
. Upon induction, both Ascl1 and Neurog2 directed morphological and immunocytochemical changes consistent with initiation of neuronal differentiation. Comparison of Ascl1- and Neurog2-regulated genes by microarray analyses showed both shared and distinct transcriptional changes for each bHLH protein. In both Ascl1- and Neurog2-differentiating cells, repression of Oct4 mRNA levels was accompanied by increased Oct4 promoter methylation. However, DNA demethylation was not detected for genes induced by either bHLH protein. Neurog2-induced genes included glutamatergic marker genes while Ascl1-induced genes included GABAergic marker genes. The Neurog2-specific induction of a gene encoding a protein phosphatase inhibitor,
Ppp1r14a
, was dependent on distinct, canonical E-box sequences within the
Ppp1r14a
promoter and the nucleotide sequences within these E-boxes were partially responsible for Neurog2-specific regulation. Our results illustrate multiple novel mechanisms by which Ascl1 and Neurog2 regulate gene repression during neuronal differentiation in P19 cells.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>25189318</pmid><doi>10.1007/s12031-014-0408-2</doi><tpages>22</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0895-8696 |
| ispartof | Journal of molecular neuroscience, 2015-03, Vol.55 (3), p.684-705 |
| issn | 0895-8696 1559-1166 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1660387919 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Animals Basic Helix-Loop-Helix Transcription Factors - metabolism Biomedical and Life Sciences Biomedicine Cancer Cell Biology Cell Line, Tumor DNA methylation Embryonal Carcinoma Stem Cells - cytology Embryonal Carcinoma Stem Cells - metabolism Gene Expression Regulation, Developmental Genes Kinases Mice Muscle Proteins - genetics Muscle Proteins - metabolism Nerve Tissue Proteins - metabolism Nervous system Neurochemistry Neurogenesis Neurology Neurons Neurons - cytology Neurons - metabolism Neurosciences Octamer Transcription Factor-3 - metabolism Phosphatase Phosphoproteins - genetics Phosphoproteins - metabolism Promoter Regions, Genetic Proteins Proteomics Transcription factors Transcription, Genetic |
| title | Transcriptional Regulatory Events Initiated by Ascl1 and Neurog2 During Neuronal Differentiation of P19 Embryonic Carcinoma Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-19T00%3A41%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Transcriptional%20Regulatory%20Events%20Initiated%20by%20Ascl1%20and%20Neurog2%20During%20Neuronal%20Differentiation%20of%20P19%20Embryonic%20Carcinoma%20Cells&rft.jtitle=Journal%20of%20molecular%20neuroscience&rft.au=Huang,%20Holly%20S.&rft.date=2015-03-01&rft.volume=55&rft.issue=3&rft.spage=684&rft.epage=705&rft.pages=684-705&rft.issn=0895-8696&rft.eissn=1559-1166&rft_id=info:doi/10.1007/s12031-014-0408-2&rft_dat=%3Cproquest_cross%3E3579731361%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1651319080&rft_id=info:pmid/25189318&rfr_iscdi=true |