This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Robertson, K A Articles by Collins, S J Search for Related Content PubMed PubMed Citation Articles by Robertson, K A Articles by Collins, S J

 Previous Article  |  Next Article 

Mol Cell Biol. 1992 September; 12(9): 3743-3749

Multiple members of the retinoic acid receptor family are capable of mediating the granulocytic differentiation of HL-60 cells.

Molecular Medicine Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.

ABSTRACT

The complex and diverse biological effects of retinoic acid (RA) are mediated through specific receptors that are members of the steroid hormone family of nuclear transcription factors. The RA receptor family consists of multiple structurally distinct RA receptors, which diverge primarily at the NH2-terminal domain. The evolutionary conservation of this divergent region in individual RA receptors among different species together with their tissue-specific patterns of expression suggest that the biological function and activity of the individual RA receptors may be confined to specific tissues. To test this hypothesis in hematopoietic cells, we used retrovirus-mediated gene transduction to introduce the RA receptors RAR-alpha, RAR-beta, and RAR-gamma as well as RXR-alpha into a mutant subclone of the HL-60 promyelocytic leukemia cell line (designated HL-60R) that is relatively resistant to RA-induced granulocytic differentiation. We found that each of these structurally distinct RA receptors could restore sensitivity of the HL-60R cells to RA. A critical threshold number of transduced receptors per cell appears to be necessary to restore this functional activity. Thus, the capability to mediate granulocytic differentiation of HL-60 cells is shared among distinctly different RA receptors.

This article has been cited by other articles:

• Taschner, S., Koesters, C., Platzer, B., Jorgl, A., Ellmeier, W., Benesch, T., Strobl, H. (2007). Down-regulation of RXR{alpha} expression is essential for neutrophil development from granulocyte/monocyte progenitors. Blood 109: 971-979 [Abstract] [Full Text]  
• Purton, L. E., Dworkin, S., Olsen, G. H., Walkley, C. R., Fabb, S. A., Collins, S. J., Chambon, P. (2006). RAR{gamma} is critical for maintaining a balance between hematopoietic stem cell self-renewal and differentiation. J. Exp. Med. 203: 1283-1293 [Abstract] [Full Text]  
• Cao, Z., Flanders, K. C., Bertolette, D., Lyakh, L. A., Wurthner, J. U., Parks, W. T., Letterio, J. J., Ruscetti, F. W., Roberts, A. B. (2003). Levels of phospho-Smad2/3 are sensors of the interplay between effects of TGF-beta and retinoic acid on monocytic and granulocytic differentiation of HL-60 cells. Blood 101: 498-507 [Abstract] [Full Text]  
• Si, J., Collins, S. J. (2002). IL-3-induced enhancement of retinoic acid receptor activity is mediated through Stat5, which physically associates with retinoic acid receptors in an IL-3-dependent manner. Blood 100: 4401-4409 [Abstract] [Full Text]  
• Wang, J., Barsky, L. W., Shum, C. H., Jong, A., Weinberg, K. I., Collins, S. J., Triche, T. J., Wu, L. (2002). Retinoid-induced G1 Arrest and Differentiation Activation Are Associated with a Switch to Cyclin-dependent Kinase-activating Kinase Hypophosphorylation of Retinoic Acid Receptor alpha. J. Biol. Chem. 277: 43369-43376 [Abstract] [Full Text]  
• Xu, Q., Konta, T., Furusu, A., Nakayama, K., Lucio-Cazana, J., Fine, L. G., Kitamura, M. (2002). Transcriptional Induction of Mitogen-activated Protein Kinase Phosphatase 1 by Retinoids. SELECTIVE ROLES OF NUCLEAR RECEPTORS AND CONTRIBUTION TO THE ANTIAPOPTOTIC EFFECT. J. Biol. Chem. 277: 41693-41700 [Abstract] [Full Text]  
• Chen, L. I., Sommer, K. M., Swisshelm, K. (2002). Downstream Codons in the Retinoic Acid Receptor beta -2 and beta -4 mRNAs Initiate Translation of a Protein Isoform That Disrupts Retinoid-activated Transcription. J. Biol. Chem. 277: 35411-35421 [Abstract] [Full Text]  
• Johnson, B. S., Mueller, L., Si, J., Collins, S. J. (2002). The cytokines IL-3 and GM-CSF regulate the transcriptional activity of retinoic acid receptors in different in vitro models of myeloid differentiation. Blood 99: 746-753 [Abstract] [Full Text]  
• Tamagawa, K., Shimizu, K., Ebine, T., Maitani, Y., Fukui, T., Kawai, K.-i., Takahashi, N. (2001). Antitumor Efficacy in Vitro and in Vivo of Falconensones, a New Type of Polyene. Clin. Cancer Res. 7: 3551-3558 [Abstract] [Full Text]  
• Robertson, K. A., Bullock, H. A., Xu, Y., Tritt, R., Zimmerman, E., Ulbright, T. M., Foster, R. S., Einhorn, L. H., Kelley, M. R. (2001). Altered Expression of Ape1/ref-1 in Germ Cell Tumors and Overexpression in NT2 Cells Confers Resistance to Bleomycin and Radiation. Cancer Res. 61: 2220-2225 [Abstract] [Full Text]  
• Shimizu, T., Takeda, K. (2000). Induction of Retinoic Acid Receptor-{{alpha}} by Granulocyte Macrophage Colony-stimulating Factor in Human Myeloid Leukemia Cell Lines. Cancer Res. 60: 4544-4549 [Abstract] [Full Text]  
• Wan, H., Oridate, N., Lotan, D., Hong, W. K., Lotan, R. (1999). Overexpression of Retinoic Acid Receptor {beta} in Head and Neck Squamous Cell Carcinoma Cells Increases Their Sensitivity to Retinoid-induced Suppression of Squamous Differentiation by Retinoids. Cancer Res. 59: 3518-3526 [Abstract] [Full Text]  
• Melnick, A., Licht, J. D. (1999). Deconstructing a Disease: RAR{alpha}, Its Fusion Partners, and Their Roles in the Pathogenesis of Acute Promyelocytic Leukemia. Blood 93: 3167-3215 [Full Text]  
• Spanjaard, R. A., Ikeda, M., Lee, P. J., Charpentier, B., Chin, W. W., Eberlein, T. J. (1997). Specific Activation of Retinoic Acid Receptors (RARs) and Retinoid X Receptors Reveals a Unique Role for RARgamma in Induction of Differentiation and Apoptosis of S91 Melanoma Cells. J. Biol. Chem. 272: 18990-18999 [Abstract] [Full Text]  
• Tenen, D. G., Hromas, R., Licht, J. D., Zhang, D.-E. (1997). Transcription Factors, Normal Myeloid Development, and Leukemia. Blood 90: 489-519 [Full Text]  
• Twining, S. S., Schulte, D. P., Wilson, P. M., Fish, B. L., Moulder, J. E. (1997). Vitamin A Deficiency Alters Rat Neutrophil Function. J. Nutr. 127: 558-565 [Abstract] [Full Text]  
• Wolfgang, C. L., Zhang, Z.-p., Gabriel, J. L., Pieringer, R. A., Soprano, K. J., Soprano, D. R. (1997). Identification of Sulfhydryl-modified Cysteine Residues in the Ligand Binding Pocket of Retinoic Acid Receptor beta. J. Biol. Chem. 272: 746-753 [Abstract] [Full Text]  
• Konta, T., Xu, Q., Furusu, A., Nakayama, K., Kitamura, M. (2001). Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid. J. Biol. Chem. 276: 12697-12701 [Abstract] [Full Text]