Source:http://linkedlifedata.com/resource/pubmed/id/12609742
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2003-2-28
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pubmed:abstractText |
The Wilms' tumor gene Wt1 encodes a zinc finger protein, which is required for normal formation of the genitourinary system and mesothelial tissues. Our recent findings indicate that Wt1 also plays a critical role in the development of ganglion cells in the vertebrate retina. Here we show that the POU-domain factor Pou4f2 (formerly Brn-3b), which is necessary for retinal ganglion cell survival, is up-regulated in human embryonic kidney (HEK)293 cells with stable Wt1 expression. Consistent with our previous observations of increased Pou4f2 mRNA in stably Wt1-transfeced HEK293 cells [EMBO J. 21 (2002) 1398], endogenous Pou4f2 was also elevated at the protein level in the HEK293 transfectants as well as in U2OS osteosarcoma cells that expressed an inducible Wt1 isoform. Transient co-transfection of a Wt1 expression construct activated a Pou4f2 promoter-reporter construct approximately 4-fold. Stimulation of the Pou4f2 promoter required a Wt1 binding element that was similar to a degenerative consensus site previously identified in other Wt1 responsive genes. Double-immunofluorescent labeling revealed co-expression of Pou4f2 and Wt1 in glomerular podocytes of adult kidney and in developing retinal ganglion cells of mouse embryos. Pou4f2 immunoreactivity was absent from the retinas of Wt1(-/-) embryos. In conclusion, we identified Pou4f2 as a novel downstream target gene of Wt1. Co-localization of both proteins in glomerular podocytes of the kidney and in developing retinal ganglion cells suggests a role for Wt1-Pou4f2 interaction in these tissues.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/POU4F2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor Brn-3,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor Brn-3B,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/WT1 Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0378-1119
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
305
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
217-23
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12609742-Animals,
pubmed-meshheading:12609742-Cell Line,
pubmed-meshheading:12609742-DNA-Binding Proteins,
pubmed-meshheading:12609742-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:12609742-Female,
pubmed-meshheading:12609742-Humans,
pubmed-meshheading:12609742-Immunoblotting,
pubmed-meshheading:12609742-Immunohistochemistry,
pubmed-meshheading:12609742-Kidney,
pubmed-meshheading:12609742-Luciferases,
pubmed-meshheading:12609742-Male,
pubmed-meshheading:12609742-Mice,
pubmed-meshheading:12609742-Mice, Inbred C57BL,
pubmed-meshheading:12609742-Protein Binding,
pubmed-meshheading:12609742-Recombinant Fusion Proteins,
pubmed-meshheading:12609742-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:12609742-Retina,
pubmed-meshheading:12609742-Transcription Factor Brn-3,
pubmed-meshheading:12609742-Transcription Factor Brn-3B,
pubmed-meshheading:12609742-Transcription Factors,
pubmed-meshheading:12609742-Transcriptional Activation,
pubmed-meshheading:12609742-Transfection,
pubmed-meshheading:12609742-Tumor Cells, Cultured,
pubmed-meshheading:12609742-WT1 Proteins
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pubmed:year |
2003
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pubmed:articleTitle |
The Wilms' tumor suppressor Wt1 encodes a transcriptional activator of the class IV POU-domain factor Pou4f2 (Brn-3b).
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pubmed:affiliation |
Johannes-Müller-Institut für Physiologie, Humboldt-Universität, Charité, Tucholskystrasse 2, 10117 Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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