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      An octamer motif contributes to the expression of the retinoic acid-regulated zinc finger gene Rex-1 (Zfp-42) in F9 teratocarcinoma cells.

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      Molecular and Cellular Biology
      American Society for Microbiology

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          Abstract

          The message for the zinc finger gene Rex-1 (Zfp-42) is expressed in undifferentiated murine F9 teratocarcinoma cells and embryonic stem cells. Expression of Rex-1 is reduced at the transcriptional level when F9 cells are induced by the addition of retinoic acid (RA) to differentiate. We have isolated genomic DNA for the Rex-1 gene (Zfp-42), characterized the gene's structure, and mapped the gene to mouse chromosome 8. Promoter elements contributing to the regulation of the Rex-1 promoter in F9 cells have been identified. A region required for Rex-1 promoter activity in F9 stem cells contains an octamer motif (ATTTGCAT) which is a binding site for octamer transcription factor members of the POU domain family of DNA-binding proteins. Rex-1 reporter plasmids including this octamer site also exhibited reduced expression in F9 cells treated with RA. Thus, the octamer motif is a regulatory element required for the activity of the Rex-1 promoter in F9 stem cells, and this motif contributes to the negative regulation by RA of the transcription of the Rex-1 gene. As an initial confirmation of the in vivo relevance of the isolated fragment, a larger Rex-1 promoter fragment, also containing the octamer site, was able to promote expression of the bacterial lacZ gene in mouse embryos at the morula stage.

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          Author and article information

          Journal
          Molecular and Cellular Biology
          Mol. Cell. Biol.
          American Society for Microbiology
          0270-7306
          1098-5549
          May 01 1993
          May 1993
          May 1993
          May 01 1993
          : 13
          : 5
          : 2919-2928
          Article
          10.1128/MCB.13.5.2919
          359685
          8474450
          c22ceef6-cff7-4418-b2ee-599696632e94
          © 1993
          History

          Molecular medicine,Neurosciences
          Molecular medicine, Neurosciences

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