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J Biol Chem, Vol. 273, Issue 33, 21210-21216, August 14, 1998

Activation-induced Down-regulation of Retinoid Receptor RXR Expression in Human T Lymphocytes
ROLE OF CELL CYCLE REGULATION

Mohammad Ishaq, Yi-Ming Zhang^¶, and Ven Natarajan

From the  Laboratory of Molecular Cell Biology and the ^¶ Laboratory of Molecular Retrovirology, SAIC-Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201

A 5.4-kilobase mRNA, the expression of which is down-regulated after treatment of human peripheral blood mononuclear cells (PBMCs) with various T cell-activating agents, was isolated using an mRNA differential display method. Nucleotide sequence analysis identified the 5' end of this RNA as human retinoid receptor RXR mRNA. Here, we report the nucleotide sequence of 3.6 kilobases of this RNA, which represents the 3' end of RXR mRNA, the sequence of which has not been previously described. Activated PBMCs also expressed lower levels of RXR protein, and a DNA binding assay showed that the activation-induced loss of RXR mRNA and protein expression correlated with the loss of DNA binding activity of this protein. We present evidence that the transition from G₀/G₁ to S phase of the cell cycle results in the down-regulation of RXR expression and that cell cycle inhibitors, which block the cells in G₁ phase, prevent this down-regulation. The decrease in the levels of RXR mRNA was found to be regulated at the post-transcriptional level and involved new protein synthesis. These observations indicate that the levels of RXR expression in T lymphocytes are coupled to cell cycle progression, and there is tight regulatory control of RXR expression during the transition from G₀/G₁ to S phase of the cell cycle.

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