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Erythroid Cell-Specific -Globin Gene Regulation by the CP2 Transcription Factor Family

Ho Chul Kang,^1, Ji Hyung Chae,^1, Yeon Ho Lee,¹ Mi-Ae Park,¹ June Ho Shin,¹ Sung-Hyun Kim,¹ Sang-Kyu Ye,² Yoon Shin Cho,¹ Steven Fiering,³ and Chul Geun Kim^1*

Department of Life Science and Research Institute for Natural Sciences, College of Natural Sciences, Hanyang University, Seoul 133-791, South Korea,¹ Department of Pharmacology, College of Medicine, Seoul National University, Seoul 110-799, South Korea,² Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, New Hampshire 03756³

Received 2 December 2004/ Returned for modification 17 January 2005/ Accepted 23 April 2005

We previously demonstrated that ubiquitously expressed CP2c exerts potent erythroid-specific transactivation of -globin through an unknown mechanism. This mechanism is reported here to involve specific CP2 splice variants and protein inhibitor of activated STAT1 (PIAS1). We identify a novel murine splice isoform of CP2, CP2b, which is identical to CP2a except that it has an additional 36 amino acids encoded by an extra exon. CP2b has an erythroid cell-specific transcriptional activation domain, which requires the extra exon and can form heteromeric complexes with other CP2 isoforms, but lacks the DNA binding activity found in CP2a and CP2c. Transcriptional activation of -globin occurred following dimerization between CP2b and CP2c in erythroid K562 and MEL cells, but this dimerization did not activate the -globin promoter in nonerythroid 293T cells, indicating that an additional erythroid factor is missing in 293T cells. PIAS1 was confirmed as a CP2 binding protein by the yeast two-hybrid screen, and expression of CP2b, CP2c, and PIAS1 in 293T cell induced -globin promoter activation. These results show that ubiquitously expressed CP2b exerts potent erythroid cell-specific -globin gene expression by complexing with CP2c and PIAS1.

H.C.K. and J.H.C. contributed equally to this study.

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