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http://purl.uniprot.org/citations/18515495http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18515495http://www.w3.org/2000/01/rdf-schema#comment"As successful generation of insulin-producing cells could be used for diabetes treatment, a concerted effort is being made to understand the molecular programs underlying islet beta-cell formation and function. The closely related MafA and MafB transcription factors are both key mammalian beta-cell regulators. MafA and MafB are co-expressed in insulin+beta-cells during embryogenesis, while in the adult pancreas only MafA is produced in beta-cells and MafB in glucagon+alpha-cells. MafB-/-animals are also deficient in insulin+ and glucagon+ cell production during embryogenesis. However, only MafA over-expression selectively induced endogenous Insulin mRNA production in cell line-based assays, while MafB specifically promoted Glucagon expression. Here, we analyzed whether these factors were sufficient to induce insulin+ and/or glucagon+ cell formation within embryonic endoderm using the chick in ovo electroporation assay. Ectopic expression of MafA, but not MafB, promoted Insulin production; however, neither MafA nor MafB were capable of inducing Glucagon. Co-electroporation of MafA with the Ngn3 transcription factor resulted in the development of more organized cell clusters containing both insulin- and glucagon-producing cells. Analysis of chimeric proteins of MafA and MafB demonstrated that chick Insulin activation depended on sequences within the MafA C-terminal DNA-binding domain. MafA was also bound to Insulin and Glucagon transcriptional control sequences in mouse embryonic pancreas and beta-cell lines. Collectively, these results demonstrate a unique ability for MafA to independently activate Insulin transcription."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.org/dc/terms/identifier"doi:10.1677/joe-08-0063"xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/author"Guo M."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/author"Stein R."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/author"Gu G."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/author"Artner I."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/author"Hang Y."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/name"J Endocrinol"xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/pages"271-279"xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/title"MafA is a dedicated activator of the insulin gene in vivo."xsd:string
http://purl.uniprot.org/citations/18515495http://purl.uniprot.org/core/volume"198"xsd:string
http://purl.uniprot.org/citations/18515495http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18515495
http://purl.uniprot.org/citations/18515495http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18515495
http://purl.uniprot.org/uniprot/#_Q3V2C2-mappedCitation-18515495http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18515495
http://purl.uniprot.org/uniprot/#_P54841-mappedCitation-18515495http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18515495
http://purl.uniprot.org/uniprot/#_Q8CF90-mappedCitation-18515495http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18515495
http://purl.uniprot.org/uniprot/P54841http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/18515495
http://purl.uniprot.org/uniprot/Q3V2C2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/18515495
http://purl.uniprot.org/uniprot/Q8CF90http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/18515495