RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15220343http://www.w3.org/2000/01/rdf-schema#comment"Laminin-1 is the major component of embryonic basement membrane and consists of alpha1, beta1, and gamma1 chains. The expression of laminin-1 is induced in mouse F9 embryonal carcinoma cells upon differentiation into parietal endoderm cells. We recently identified a parietal endoderm-specific enhancer in the mouse laminin alpha1 (Lama1) gene and showed that Sp1/Sp3 and YY1 transcription factors were involved in the enhancer activity. Although here we identified that NF-Y binds to the enhancer sequence between Sp1/Sp3- and YY1-binding sites, all these transcription factors are ubiquitously expressed and thus are not sufficient to explain parietal endoderm-specific enhancer activity. In the present study, we further showed that SOX7 and SOX17 are involved in the regulation of parietal endoderm-specific enhancer activity of the mouse Lama1 gene. Northern blot analysis revealed that the steady-state levels of mouse Sox7 and Sox17 mRNAs increased in parallel with that of Lama1 mRNA during the differentiation of F9 cells. Both SOX7 and SOX17 markedly trans-activated the transcription of the Lama1 enhancer-reporter construct in undifferentiated F9 cells in a manner dependent on high mobility group box-mediated DNA binding. Electrophoretic mobility shift assays and mutational analyses revealed that SOX7 and SOX17 bound specifically to two SOX-binding sites within the Lama1 enhancer, and that these SOX-binding sites functioned synergistically to confer the trans-activation by SOX7 and SOX17. Furthermore, this trans-activation was dependent on the integrity of the binding sites for Sp1/Sp3 and NF-Y located at upstream of the two SOX-binding sites. These results indicate that the transcription of the mouse Lama1 gene during the differentiation of F9 cells is controlled by a combination of the actions of the ubiquitous factors, Sp1/Sp3 and NF-Y, and the parietal endoderm-specific factors, SOX7 and SOX17."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m403724200"xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/author"Futaki S."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/author"Hayashi Y."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/author"Sekiguchi K."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/author"Niimi T."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/pages"38055-38061"xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/title"SOX7 and SOX17 regulate the parietal endoderm-specific enhancer activity of mouse laminin alpha1 gene."xsd:string
http://purl.uniprot.org/citations/15220343http://purl.uniprot.org/core/volume"279"xsd:string
http://purl.uniprot.org/citations/15220343http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15220343
http://purl.uniprot.org/citations/15220343http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15220343
http://purl.uniprot.org/uniprot/P63139#attribution-37BB356B3F1A4B4DF489EDEEA93F7302http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/Q61473#attribution-37BB356B3F1A4B4DF489EDEEA93F7302http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/P40646#attribution-37BB356B3F1A4B4DF489EDEEA93F7302http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_A0A0A6YWS4-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_A0A0A6YXS3-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_A0A0A6YXV3-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_A0A0A6YXZ2-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_D3Z723-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_Q3U0W9-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_Q61473-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343
http://purl.uniprot.org/uniprot/#_P19137-mappedCitation-15220343http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15220343