Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis

Chih Hao Lee; Li Na Wei

doi:10.1016/S0006-2952(00)00311-7

Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis

Chih Hao Lee, Li Na Wei

Pharmacology

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

The complete mouse orphan nuclear receptor TR2-11 gene structure and its 5'-untranscribed region were characterized. This gene contains 14 exons, with the first exon encoding only the 5'-untranslated sequence. The regulatory region of this gene was characterized by using reporter assays that define the minimal promoter activity in a sequence 212 nucleotides upstream from the translation initiation site. Furthermore, it was concluded that splicing of intron 1 is required for efficient promoter activity. Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-α (RAR(α)) and retinoid receptor X-β (RXR(β))._. Binding of RAR(α)/RXR(β) to the minimal promoter region was demonstrated in gel retardation assays. In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Copyright (C) 2000 Elsevier Science Inc.

Original language	English (US)
Pages (from-to)	127-136
Number of pages	10
Journal	Biochemical Pharmacology
Volume	60
Issue number	1
DOIs	https://doi.org/10.1016/S0006-2952(00)00311-7
State	Published - Jul 2000

Bibliographical note

Funding Information:
This work was supported by a leukemia research fund from the University of Minnesota, USDA/98–35200–6264 from USDA, RPG-99–238-01-CNE from ACS, and DK54733 from NIDDK to L-N. W. We thank members of Dr. Horace Loh’s laboratory and Hung-Chun Chen for assistance and for the one-paired t-test analysis, and we acknowledge the help of Dr. X. Hu in RT–PCR analyses of the P19 cultures. We also thank Julie Pribyl for help in FACS analyses provided by the Cancer Center Flow Cytometry Core Facility of the University of Minnesota.

Keywords

Apoptosis
Orphan receptor
P19 embryonal carcinoma cells
Retinoic acid
TR2-11 expression
TR2-11 gene

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10.1016/S0006-2952(00)00311-7

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title = "Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis",

abstract = "The complete mouse orphan nuclear receptor TR2-11 gene structure and its 5'-untranscribed region were characterized. This gene contains 14 exons, with the first exon encoding only the 5'-untranslated sequence. The regulatory region of this gene was characterized by using reporter assays that define the minimal promoter activity in a sequence 212 nucleotides upstream from the translation initiation site. Furthermore, it was concluded that splicing of intron 1 is required for efficient promoter activity. Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-α (RAR(α)) and retinoid receptor X-β (RXR(β)).. Binding of RAR(α)/RXR(β) to the minimal promoter region was demonstrated in gel retardation assays. In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Copyright (C) 2000 Elsevier Science Inc.",

keywords = "Apoptosis, Orphan receptor, P19 embryonal carcinoma cells, Retinoic acid, TR2-11 expression, TR2-11 gene",

author = "Lee, {Chih Hao} and Wei, {Li Na}",

note = "Funding Information: This work was supported by a leukemia research fund from the University of Minnesota, USDA/98–35200–6264 from USDA, RPG-99–238-01-CNE from ACS, and DK54733 from NIDDK to L-N. W. We thank members of Dr. Horace Loh{\textquoteright}s laboratory and Hung-Chun Chen for assistance and for the one-paired t-test analysis, and we acknowledge the help of Dr. X. Hu in RT–PCR analyses of the P19 cultures. We also thank Julie Pribyl for help in FACS analyses provided by the Cancer Center Flow Cytometry Core Facility of the University of Minnesota.",

year = "2000",

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doi = "10.1016/S0006-2952(00)00311-7",

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AU - Lee, Chih Hao

AU - Wei, Li Na

N1 - Funding Information: This work was supported by a leukemia research fund from the University of Minnesota, USDA/98–35200–6264 from USDA, RPG-99–238-01-CNE from ACS, and DK54733 from NIDDK to L-N. W. We thank members of Dr. Horace Loh’s laboratory and Hung-Chun Chen for assistance and for the one-paired t-test analysis, and we acknowledge the help of Dr. X. Hu in RT–PCR analyses of the P19 cultures. We also thank Julie Pribyl for help in FACS analyses provided by the Cancer Center Flow Cytometry Core Facility of the University of Minnesota.

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N2 - The complete mouse orphan nuclear receptor TR2-11 gene structure and its 5'-untranscribed region were characterized. This gene contains 14 exons, with the first exon encoding only the 5'-untranslated sequence. The regulatory region of this gene was characterized by using reporter assays that define the minimal promoter activity in a sequence 212 nucleotides upstream from the translation initiation site. Furthermore, it was concluded that splicing of intron 1 is required for efficient promoter activity. Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-α (RAR(α)) and retinoid receptor X-β (RXR(β)).. Binding of RAR(α)/RXR(β) to the minimal promoter region was demonstrated in gel retardation assays. In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Copyright (C) 2000 Elsevier Science Inc.

AB - The complete mouse orphan nuclear receptor TR2-11 gene structure and its 5'-untranscribed region were characterized. This gene contains 14 exons, with the first exon encoding only the 5'-untranslated sequence. The regulatory region of this gene was characterized by using reporter assays that define the minimal promoter activity in a sequence 212 nucleotides upstream from the translation initiation site. Furthermore, it was concluded that splicing of intron 1 is required for efficient promoter activity. Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-α (RAR(α)) and retinoid receptor X-β (RXR(β)).. Binding of RAR(α)/RXR(β) to the minimal promoter region was demonstrated in gel retardation assays. In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Copyright (C) 2000 Elsevier Science Inc.

KW - Apoptosis

KW - Orphan receptor

KW - P19 embryonal carcinoma cells

KW - Retinoic acid

KW - TR2-11 expression

KW - TR2-11 gene

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JF - Biochemical Pharmacology

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ER -

Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis

Abstract

Bibliographical note

Keywords

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