scholarly journals Retinoic Acid Down-regulation of Fibronectin and Retinoic Acid Receptor Proteins in NIH-3T3 Cells

1996 ◽  
Vol 271 (11) ◽  
pp. 6502-6508 ◽  
Author(s):  
Giorgio Scita ◽  
Nadine Darwiche ◽  
Eileen Greenwald ◽  
Miriam Rosenberg ◽  
Katerina Politi ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
3T3 Cells ◽  
Down Regulation ◽  
Acid Receptor ◽  
Receptor Proteins ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.

1995 ◽  
Vol 181 (6) ◽  
pp. 1965-1973 ◽  
Author(s):  
J H Liu ◽  
Z M Mu ◽  
K S Chang
Keyword(s):  
Retinoic Acid Receptor ◽  
Normal Function ◽  
Critical Event ◽  
Cell Cycle Distribution ◽  
3T3 Cells ◽  
Stable Transfectants ◽  
Neu Oncogene ◽  
Nih 3T3 ◽  
Growth Suppressor ◽  
Nih 3T3 Cells

The chromosomal translocation t(15;17)(q22;q12) is a consistent feature of acute promyelocytic leukemia (APL) that results in the disruption of genes for the zinc finger transcription factor PML and the retinoic acid receptor alpha (RAR alpha). We have previously shown that PML is a growth suppressor and is able to suppress transformation of NIH/3T3 by activated neu oncogene. In the study presented here, the full-length PML cDNA was transfected into B104-1-1 cells (NIH/3T3 cells transformed by the activated neu oncogene) by retrovirally mediated gene transfer. We found that expression of PML could reverse phenotypes of B104-1-1 including morphology, contact-limiting properties, and growth rate in both transient-expression and stable transfectants. We also demonstrated that PML is able to suppress clonogenicity of B104-1-1 in soft agar assay and tumorigenicity in nude mice. These results strongly support our previous finding that PML is a transformation or growth suppressor. Our results further demonstrate that expression of PML in B104-1-1 cells has little effect on cell cycle distribution. Western blot analysis demonstrated that suppression of neu expression in B104-1-1 by PML was insignificant in the transient transfection experiment but significant in the PML stable transfectants. This study suggests that PML may suppress neu expression and block signaling events associated with activated neu. This study supports our hypothesis that disruption of the normal function of PML, a growth or transformation suppressor, is a critical event in APL leukomogenesis.

scholarly journals Down-regulation of Retinoic Acid Receptor α Signaling Is Required for Sacculation and Type I Cell Formation in the Developing Lung

2003 ◽  
Vol 278 (47) ◽  
pp. 46911-46918 ◽  
Author(s):  
Cherry Wongtrakool ◽  
Sarah Malpel ◽  
Julie Gorenstein ◽  
Jeff Sedita ◽  
Maria I. Ramirez ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Cell Formation ◽  
Type I ◽  
Down Regulation ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Α

scholarly journals The T-Cell Oncogenic Protein HOX11 ActivatesAldh1 Expression in NIH 3T3 Cells but Represses Its Expression in Mouse Spleen Development

1998 ◽  
Vol 18 (12) ◽  
pp. 7030-7037 ◽  
Author(s):  
Wayne K. Greene ◽  
Sabine Bahn ◽  
Norma Masson ◽  
Terence H. Rabbitts
Keyword(s):  
Retinoic Acid ◽  
T Cell ◽  
Target Genes ◽  
Representational Difference Analysis ◽  
Null Mouse ◽  
Cdna Clones ◽  
3T3 Cells ◽  
Acute Leukemias ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

ABSTRACT Hox11 is a homeobox gene essential for spleen formation in mice, since atrophy of the anlage of a developing spleen occurs in early embryonic development in Hox11 null mice. HOX11 is also expressed in a subset of T-cell acute leukemias after specific chromosomal translocations. Since the protein has a homeodomain and can activate transcription, it probably exerts at least some of its effects in vivo by regulation of target genes. Representational difference analysis has been used to isolate cDNA clones corresponding to mRNA species activated following stable expression of HOX11 in NIH 3T3 cells. The gene encoding the retinoic acid-synthesizing enzyme aldehyde dehydrogenase 1 (Aldh1), initially called Hdg-1, was found to be ectopically activated by HOX11 in this system. Study ofAldh1 gene expression during spleen development showed that the presence of Aldh1 mRNA inversely correlated withHox11. Hox11 null mouse embryos have elevatedAldh1 mRNA in spleen primordia prior to atrophy, whileAldh1 seems to be repressed by Hox11 during organogenesis of the spleens of wild-type mice. This result suggests that expression of Aldh1 protein is negatively regulated by Hox11 and that abnormal expression of Aldh1 in Hox11 null mice may cause loss of splenic precursor cells by aberrant retinoic acid metabolism.

Effect of dexamethasone and oxygen exposure on neonatal rat lung retinoic acid receptor proteins

1994 ◽  
Vol 18 (4) ◽  
pp. 232-238 ◽  
Author(s):  
Kandi R. McMenamy ◽  
Marni J. Anderson ◽  
Richard D. Zachman
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Neonatal Rat ◽  
Rat Lung ◽  
Acid Receptor ◽  
Receptor Proteins ◽  
Oxygen Exposure

Contribution of retinoic acid receptor signalling to adrenal cortex morphology and functional zonation through modulation of WNT/[beta]-catenin pathway

2017 ◽  
Author(s):  
Zein Rami El ◽  
Amanda J Rickard ◽  
Golib Dzib Jose Felipe ◽  
Benoit Samson-Couterie ◽  
Angelique Rocha ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Adrenal Cortex ◽  
Retinoic Acid Receptor ◽  
Beta Catenin ◽  
Acid Receptor ◽  
Receptor Signalling
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