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http://purl.uniprot.org/citations/24469635http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24469635http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24469635http://www.w3.org/2000/01/rdf-schema#comment"The unique functional properties and molecular identity of neuronal cell populations rely on cell type-specific gene expression programs. Alternative splicing represents a powerful mechanism for expanding the capacity of genomes to generate molecular diversity. Neuronal cells exhibit particularly extensive alternative splicing regulation. We report a highly selective expression of the KH domain-containing splicing regulators SLM1 and SLM2 in the mouse brain. Conditional ablation of SLM1 resulted in a severe defect in the neuronal isoform content of the polymorphic synaptic receptors neurexin-1, -2, and -3. Thus, cell type-specific expression of SLM1 provides a mechanism for shaping the molecular repertoires of synaptic adhesion molecules in neuronal populations in vivo."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.org/dc/terms/identifier"doi:10.1083/jcb.201310136"xsd:string
http://purl.uniprot.org/citations/24469635http://purl.org/dc/terms/identifier"doi:10.1083/jcb.201310136"xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Iijima Y."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Iijima Y."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Witte H."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Witte H."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Iijima T."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Iijima T."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Scheiffele P."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/author"Scheiffele P."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/name"J. Cell Biol."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/name"J. Cell Biol."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/pages"331-342"xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/pages"331-342"xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/title"Neuronal cell type-specific alternative splicing is regulated by the KH domain protein SLM1."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/title"Neuronal cell type-specific alternative splicing is regulated by the KH domain protein SLM1."xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/volume"204"xsd:string
http://purl.uniprot.org/citations/24469635http://purl.uniprot.org/core/volume"204"xsd:string
http://purl.uniprot.org/citations/24469635http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24469635
http://purl.uniprot.org/citations/24469635http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24469635