scholarly journals Retardation of skeletal development and cervical abnormalities in transgenic mice expressing a dominant-negative retinoic acid receptor in chondrogenic cells

1998 ◽  
Vol 95 (13) ◽  
pp. 7491-7496 ◽  
Author(s):  
M. Yamaguchi ◽  
M. Nakamoto ◽  
H. Honda ◽  
T. Nakagawa ◽  
H. Fujita ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Transgenic Mice ◽  
Retinoic Acid Receptor ◽  
Skeletal Development ◽  
Dominant Negative ◽  
Acid Receptor

scholarly journals Retinoic acid receptor ? dominant negative form causes steatohepatitis and liver tumors in transgenic mice

Hepatology ◽  
2004 ◽  
Vol 40 (2) ◽  
pp. 366-375 ◽  
Author(s):  
Atsushi Yanagitani ◽  
Sadako Yamada ◽  
Sakiko Yasui ◽  
Takashi Shimomura ◽  
Rie Murai ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Transgenic Mice ◽  
Liver Tumors ◽  
Retinoic Acid Receptor ◽  
Dominant Negative ◽  
Acid Receptor ◽  
Dominant Negative Form ◽  
Negative Form

scholarly journals Male Infertility Caused by Epididymal Dysfunction in Transgenic Mice Expressing a Dominant Negative Mutation of Retinoic Acid Receptor α1

1997 ◽  
Vol 56 (4) ◽  
pp. 985-990 ◽  
Author(s):  
Stacy L. Costa ◽  
Kim Boekelheide ◽  
Barbara C. Vanderhyden ◽  
Rahul Seth ◽  
Michael W. McBurney
Keyword(s):  
Retinoic Acid ◽  
Male Infertility ◽  
Transgenic Mice ◽  
Retinoic Acid Receptor ◽  
Dominant Negative ◽  
Acid Receptor ◽  
Dominant Negative Mutation

scholarly journals Targeting expression of a dominant-negative retinoic acid receptor mutant in the epidermis of transgenic mice results in loss of barrier function.

1995 ◽  
Vol 9 (3) ◽  
pp. 317-329 ◽  
Author(s):  
S Imakado ◽  
J R Bickenbach ◽  
D S Bundman ◽  
J A Rothnagel ◽  
P S Attar ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Transgenic Mice ◽  
Barrier Function ◽  
Retinoic Acid Receptor ◽  
Dominant Negative ◽  
Acid Receptor ◽  
Receptor Mutant

Expression of a dominant negative retinoic acid receptor ? in Xenopus embryos leads to partial resistance to retinoic acid

1994 ◽  
Vol 203 (5) ◽  
pp. 254-265 ◽  
Author(s):  
Darrin Paul Smith ◽  
Clive Scott Mason ◽  
Elizabeth Jones ◽  
Robert Old
Keyword(s):  
Retinoic Acid ◽  
Partial Resistance ◽  
Retinoic Acid Receptor ◽  
Dominant Negative ◽  
Acid Receptor ◽  
Xenopus Embryos

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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