scholarly journals Dominant-Negative Nuclear Receptor Corepressor Relieves Transcriptional Inhibition of Retinoic Acid Receptor but Does Not Alter the Agonist/Antagonist Activities of the Tamoxifen-Bound Estrogen Receptor

2003 ◽  
Vol 17 (8) ◽  
pp. 1543-1554 ◽  
Author(s):  
Ashby J. Morrison ◽  
Rafael E. Herrera ◽  
Ester Coronado Heinsohn ◽  
Rachel Schiff ◽  
C. Kent Osborne
Keyword(s):  
Estrogen Receptor ◽  
Retinoic Acid ◽  
Nuclear Receptor ◽  
Retinoic Acid Receptor ◽  
Dominant Negative ◽  
Acid Receptor ◽  
Transcriptional Inhibition ◽  
Nuclear Receptor Corepressor

scholarly journals Recruitment of Nuclear Receptor Corepressor and Coactivator to the Retinoic Acid Receptor by Retinoid Ligands

2000 ◽  
Vol 275 (25) ◽  
pp. 19401-19408 ◽  
Author(s):  
Elliott S. Klein ◽  
Jenny W. Wang ◽  
Berket Khalifa ◽  
Stacey A. Gavigan ◽  
Roshantha A. S. Chandraratna
Keyword(s):  
Retinoic Acid ◽  
Nuclear Receptor ◽  
Retinoic Acid Receptor ◽  
Acid Receptor ◽  
Nuclear Receptor Corepressor

Retinoic acid-resistant HL-60 cells exclusively contain mutant retinoic acid receptor-alpha

Blood ◽  
1994 ◽  
Vol 83 (11) ◽  
pp. 3298-3302 ◽  
Author(s):  
YP Li ◽  
F Said ◽  
RE Gallagher
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Hot Spot ◽  
Dominant Negative ◽  
Reaction Products ◽  
Retinoic Acid Receptor Alpha ◽  
Restriction Endonuclease Site ◽  
Acid Receptor ◽  
Receptor Alpha ◽  
Alpha Gene

Abstract Sequence analysis of the retinoic acid receptor-alpha (RAR alpha) gene from a subline of HL-60 cells (RA-res) stably resistant to all-trans retinoic acid (RA) disclosed a single-base change in codon number 411, the same C to T transition previously reported in an independently selected HL-60 RA resistant clone by Robertson et al (Blood 80:1885, 1992). This mutation eliminates a FokI restriction endonuclease site. Using primers framing this mutation in exon 9 of the RAR alpha gene, we showed that polymerase chain reaction products amplified from either mRNA or genomic DNA templates from the RA-res subline were completely resistant to FokI digestion whereas those from wild-type (wt) HL-60 cells could be digested to completion. The lack of a normal allele in the RA-res cells was confirmed by mixing experiments and hybridization analyses. Southern blot analysis of DNA from the RA-res and wt cells versus control placental DNA indicated that the RAR alpha gene is not haploid. The independent isolation of the same RAR alpha mutation in different laboratories suggests either that the mutation exits in a small subpopulation in the wt line or that this is a mutational “hot spot.” Furthermore, the results indicate that if a dominant negative mode of resistance is involved in the RA-res subline, this must involve interference with the function of heterologous receptor proteins such as the retinoid X receptors. The lack of any normal RAR alpha in this subline may facilitate studies of the mode of action of retinoids.

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