A splice variant of Dp71 lacking the syntrophin binding site is expressed in early stages of human neural development
Dp71, a 71 kDa C-terminal isoform of dystrophin, is the major product of the DMD gene in brain. Two alternatively spliced transcripts of Dp71 were amplified by RT-PCR from different areas of human fetal neural tissue. Both transcripts were spliced out of exons 71 and 78. The shorter transcript was a...
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| Veröffentlicht in: | Brain research. Developmental brain research 1997-10, Vol.103 (1), p.77-82 |
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| container_title | Brain research. Developmental brain research |
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| creator | Ceccarini, Marina Rizzo, Giovanni Rosa, Giuseppina Chelucci, Cristiana Macioce, Pompeo Petrucci, Tamara C |
| description | Dp71, a 71 kDa C-terminal isoform of dystrophin, is the major product of the DMD gene in brain. Two alternatively spliced transcripts of Dp71 were amplified by RT-PCR from different areas of human fetal neural tissue. Both transcripts were spliced out of exons 71 and 78. The shorter transcript was also alternatively spliced of exons 72–74, a region comprising the coding sequence for the binding site to syntrophin, one component of the dystrophin-associated protein complex. Results indicate that alternatively spliced forms of Dp71 are regulated during human neural development. |
| doi_str_mv | 10.1016/S0165-3806(97)00122-3 |
| format | Article |
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Two alternatively spliced transcripts of Dp71 were amplified by RT-PCR from different areas of human fetal neural tissue. Both transcripts were spliced out of exons 71 and 78. The shorter transcript was also alternatively spliced of exons 72–74, a region comprising the coding sequence for the binding site to syntrophin, one component of the dystrophin-associated protein complex. Results indicate that alternatively spliced forms of Dp71 are regulated during human neural development.</description><identifier>ISSN: 0165-3806</identifier><identifier>DOI: 10.1016/S0165-3806(97)00122-3</identifier><identifier>PMID: 9370062</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alternative Splicing ; Apo-dystrophin 1 ; Binding Sites ; Brain - embryology ; Brain - metabolism ; Dp71 ; Duchenne muscular dystrophy ; Dystrophin - analogs & derivatives ; Dystrophin - biosynthesis ; Dystrophin - genetics ; Dystrophin - metabolism ; Dystrophin-Associated Proteins ; Embryonic and Fetal Development ; Exons ; Gene Expression Regulation, Developmental ; Genetic Variation ; Human ; Humans ; Membrane Proteins - metabolism ; Muscle Proteins - metabolism ; Nervous system development ; Polymerase Chain Reaction ; Recombinant Proteins - biosynthesis ; Recombinant Proteins - metabolism ; Transcription, Genetic</subject><ispartof>Brain research. Developmental brain research, 1997-10, Vol.103 (1), p.77-82</ispartof><rights>1997 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-98a8f40e0f247b29e5fb8c9bb0d64a0483dd3102ce8f69a21b947f493630a5573</citedby><cites>FETCH-LOGICAL-c457t-98a8f40e0f247b29e5fb8c9bb0d64a0483dd3102ce8f69a21b947f493630a5573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9370062$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ceccarini, Marina</creatorcontrib><creatorcontrib>Rizzo, Giovanni</creatorcontrib><creatorcontrib>Rosa, Giuseppina</creatorcontrib><creatorcontrib>Chelucci, Cristiana</creatorcontrib><creatorcontrib>Macioce, Pompeo</creatorcontrib><creatorcontrib>Petrucci, Tamara C</creatorcontrib><title>A splice variant of Dp71 lacking the syntrophin binding site is expressed in early stages of human neural development</title><title>Brain research. Developmental brain research</title><addtitle>Brain Res Dev Brain Res</addtitle><description>Dp71, a 71 kDa C-terminal isoform of dystrophin, is the major product of the DMD gene in brain. Two alternatively spliced transcripts of Dp71 were amplified by RT-PCR from different areas of human fetal neural tissue. Both transcripts were spliced out of exons 71 and 78. The shorter transcript was also alternatively spliced of exons 72–74, a region comprising the coding sequence for the binding site to syntrophin, one component of the dystrophin-associated protein complex. Results indicate that alternatively spliced forms of Dp71 are regulated during human neural development.</description><subject>Alternative Splicing</subject><subject>Apo-dystrophin 1</subject><subject>Binding Sites</subject><subject>Brain - embryology</subject><subject>Brain - metabolism</subject><subject>Dp71</subject><subject>Duchenne muscular dystrophy</subject><subject>Dystrophin - analogs & derivatives</subject><subject>Dystrophin - biosynthesis</subject><subject>Dystrophin - genetics</subject><subject>Dystrophin - metabolism</subject><subject>Dystrophin-Associated Proteins</subject><subject>Embryonic and Fetal Development</subject><subject>Exons</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Genetic Variation</subject><subject>Human</subject><subject>Humans</subject><subject>Membrane Proteins - metabolism</subject><subject>Muscle Proteins - metabolism</subject><subject>Nervous system development</subject><subject>Polymerase Chain Reaction</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>Recombinant Proteins - metabolism</subject><subject>Transcription, Genetic</subject><issn>0165-3806</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU1P3TAQ9KHVK6X9CUg-oXIIteMkjk8VgrZUQuoBOFuOveG5JE7wOk99_x6_D3HlsLvSzuysNEPIGWeXnPHm-31udSFa1nxT8oIxXpaF-EBO3tafyGfEfywjouUrslJCMtaUJ2S5ojgP3gLdmOhNSHTq6c0sOR2MffbhiaY1UNyGFKd57QPtfHC7NfoE1COF_3MERHA0g2DisKWYzBPgTmi9jCbQAEs0A3WwgWGaRwjpC_nYmwHh63GeksdfPx-ub4u7v7__XF_dFbaqZSpUa9q-YsD6spJdqaDuu9aqrmOuqQyrWuGc4Ky00PaNMiXvVCX7SolGMFPXUpyS84PuHKeXBTDp0aOFYTABpgW1VBUXMtd7RN6UXGXLMrE-EG2cECP0eo5-NHGrOdO7LPQ-C70zXSup91loke_Ojg-WbgT3dnUMIuM_DjhkOzYeokbrIVhwPoJN2k3-nQ-vCYybVw</recordid><startdate>19971020</startdate><enddate>19971020</enddate><creator>Ceccarini, Marina</creator><creator>Rizzo, Giovanni</creator><creator>Rosa, Giuseppina</creator><creator>Chelucci, Cristiana</creator><creator>Macioce, Pompeo</creator><creator>Petrucci, Tamara C</creator><general>Elsevier 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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19971020</creationdate><title>A splice variant of Dp71 lacking the syntrophin binding site is expressed in early stages of human neural development</title><author>Ceccarini, Marina ; Rizzo, Giovanni ; Rosa, Giuseppina ; Chelucci, Cristiana ; Macioce, Pompeo ; Petrucci, Tamara C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-98a8f40e0f247b29e5fb8c9bb0d64a0483dd3102ce8f69a21b947f493630a5573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Alternative Splicing</topic><topic>Apo-dystrophin 1</topic><topic>Binding Sites</topic><topic>Brain - embryology</topic><topic>Brain - metabolism</topic><topic>Dp71</topic><topic>Duchenne muscular dystrophy</topic><topic>Dystrophin - analogs & derivatives</topic><topic>Dystrophin - biosynthesis</topic><topic>Dystrophin - genetics</topic><topic>Dystrophin - metabolism</topic><topic>Dystrophin-Associated Proteins</topic><topic>Embryonic and Fetal Development</topic><topic>Exons</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Genetic Variation</topic><topic>Human</topic><topic>Humans</topic><topic>Membrane Proteins - metabolism</topic><topic>Muscle Proteins - metabolism</topic><topic>Nervous system development</topic><topic>Polymerase Chain Reaction</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>Recombinant Proteins - metabolism</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ceccarini, Marina</creatorcontrib><creatorcontrib>Rizzo, Giovanni</creatorcontrib><creatorcontrib>Rosa, Giuseppina</creatorcontrib><creatorcontrib>Chelucci, Cristiana</creatorcontrib><creatorcontrib>Macioce, Pompeo</creatorcontrib><creatorcontrib>Petrucci, Tamara C</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Brain research. Developmental brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ceccarini, Marina</au><au>Rizzo, Giovanni</au><au>Rosa, Giuseppina</au><au>Chelucci, Cristiana</au><au>Macioce, Pompeo</au><au>Petrucci, Tamara C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A splice variant of Dp71 lacking the syntrophin binding site is expressed in early stages of human neural development</atitle><jtitle>Brain research. Developmental brain research</jtitle><addtitle>Brain Res Dev Brain Res</addtitle><date>1997-10-20</date><risdate>1997</risdate><volume>103</volume><issue>1</issue><spage>77</spage><epage>82</epage><pages>77-82</pages><issn>0165-3806</issn><abstract>Dp71, a 71 kDa C-terminal isoform of dystrophin, is the major product of the DMD gene in brain. Two alternatively spliced transcripts of Dp71 were amplified by RT-PCR from different areas of human fetal neural tissue. Both transcripts were spliced out of exons 71 and 78. The shorter transcript was also alternatively spliced of exons 72–74, a region comprising the coding sequence for the binding site to syntrophin, one component of the dystrophin-associated protein complex. Results indicate that alternatively spliced forms of Dp71 are regulated during human neural development.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>9370062</pmid><doi>10.1016/S0165-3806(97)00122-3</doi><tpages>6</tpages></addata></record> |
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| ispartof | Brain research. Developmental brain research, 1997-10, Vol.103 (1), p.77-82 |
| issn | 0165-3806 |
| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Alternative Splicing Apo-dystrophin 1 Binding Sites Brain - embryology Brain - metabolism Dp71 Duchenne muscular dystrophy Dystrophin - analogs & derivatives Dystrophin - biosynthesis Dystrophin - genetics Dystrophin - metabolism Dystrophin-Associated Proteins Embryonic and Fetal Development Exons Gene Expression Regulation, Developmental Genetic Variation Human Humans Membrane Proteins - metabolism Muscle Proteins - metabolism Nervous system development Polymerase Chain Reaction Recombinant Proteins - biosynthesis Recombinant Proteins - metabolism Transcription, Genetic |
| title | A splice variant of Dp71 lacking the syntrophin binding site is expressed in early stages of human neural development |
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