Abstract

TR3 orphan receptor is a human homologue of the mouse nur77, N10 and rat NGF1-B, TIS1 genes which may represent an early response gene involved in the control of cell proliferation. We have studied potential target genes for TR3 orphan receptor using the DNA-binding domain replacement method. We found that mouse mammary tumor virus long terminal repeat-linked chloramphenicol acetyltransferase expression can be activated in transfected cells by a chimeric androgen receptor/TR3 orphan receptor/androgen receptor construct (AR/TR3/AR) in the presence of androgen. By deletion analysis, a region with 20 nucleotides in length between positions −1178 and −1159 of the mouse mammary tumor virus long terminal repeat was confirmed as a potential TR3 orphan receptor response element. These results suggest the feasibility of using the DNA-binding domain replacement method to detect target sequences of orphan receptors.

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