scholarly journals The AF-1 and AF-2 Activating Domains of Retinoic Acid Receptor-α (RARα) and Their Phosphorylation Are Differentially Involved in Parietal Endodermal Differentiation of F9 Cells and Retinoid-Induced Expression of Target Genes

2000 ◽  
Vol 14 (9) ◽  
pp. 1398-1410
Author(s):  
Cécile Rochette-Egly ◽  
Jean-Luc Plassat ◽  
Reshma Taneja ◽  
Pierre Chambon
Keyword(s):  
Retinoic Acid ◽  
Target Genes ◽  
Retinoic Acid Receptor ◽  
Induced Expression ◽  
F9 Cells ◽  
Acid Receptor ◽  
Endodermal Differentiation ◽  
Retinoic Acid Receptor Α

scholarly journals Potentiation of GATA-2 Activity through Interactions with the Promyelocytic Leukemia Protein (PML) and the t(15;17)-Generated PML-Retinoic Acid Receptor α Oncoprotein

2000 ◽  
Vol 20 (17) ◽  
pp. 6276-6286 ◽  
Author(s):  
Shinobu Tsuzuki ◽  
Masayuki Towatari ◽  
Hidehiko Saito ◽  
Tariq Enver
Keyword(s):  
Retinoic Acid ◽  
Cell Fate ◽  
Target Genes ◽  
Retinoic Acid Receptor ◽  
Promyelocytic Leukemia ◽  
Promyelocytic Leukemia Protein ◽  
Acid Receptor ◽  
Survival And Growth ◽  
Retinoic Acid Receptor Α ◽  
Zinc Finger Region

ABSTRACT The hematopoietically expressed GATA family of transcription factors function as key regulators of blood cell fate. Among these, GATA-2 is implicated in the survival and growth of multipotential progenitors. Here we report that the promyelocytic leukemia protein (PML) can complex with GATA-2 and potentiate its transactivation capacity. The binding is mediated through interaction of the zinc finger region of GATA-2 and the B-box domain of PML. The B-box region of PML is retained in the PML-RARα (retinoic acid receptor alpha) fusion protein generated by the t(15;17) translocation characteristic of acute promyelocytic leukemia (APL). Consistent with this, we provide evidence that GATA-2 can physically associate with PML-RARα. Functional experiments further demonstrated that this interaction has the capacity to render GATA-dependent transcription inducible by retinoic acid, raising the possibility that GATA target genes may be involved in the molecular pathogenesis of APL.

Retinoic Acid Inhibits Nitric Oxide Synthase-2 Expression through the Retinoic Acid Receptor-α

2000 ◽  
Vol 270 (3) ◽  
pp. 846-851 ◽  
Author(s):  
Allan Sirsjö ◽  
Andreas C Gidlöf ◽  
Anneli Olsson ◽  
Hans Törmä ◽  
Mikko Ares ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Retinoic Acid ◽  
Nitric Oxide Synthase ◽  
Retinoic Acid Receptor ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Α ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

Identification of Highly Potent Retinoic Acid Receptor α-Selective Antagonists

1997 ◽  
Vol 40 (16) ◽  
pp. 2445-2451 ◽  
Author(s):  
Min Teng ◽  
Tien T. Duong ◽  
Alan T. Johnson ◽  
Elliott S. Klein ◽  
Liming Wang ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Acid Receptor ◽  
Selective Antagonists ◽  
Retinoic Acid Receptor Α
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