scholarly journals Retinoid X Receptor Agonists Modulate Foxp3+ Regulatory T Cell and Th17 Cell Differentiation with Differential Dependence on Retinoic Acid Receptor Activation

2013 ◽  
Vol 191 (7) ◽  
pp. 3725-3733 ◽  
Author(s):  
Hajime Takeuchi ◽  
Aya Yokota-Nakatsuma ◽  
Yoshiharu Ohoka ◽  
Hiroyuki Kagechika ◽  
Chieko Kato ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
T Cell ◽  
Regulatory T Cell ◽  
Th17 Cell ◽  
Retinoic Acid Receptor ◽  
Receptor Activation ◽  
Retinoid X Receptor ◽  
Acid Receptor ◽  
Th17 Cell Differentiation

scholarly journals Retinoic acid disrupts the Golgi apparatus and increases the cytosolic routing of specific protein toxins.

1994 ◽  
Vol 125 (4) ◽  
pp. 743-753 ◽  
Author(s):  
Y N Wu ◽  
M Gadina ◽  
J H Tao-Cheng ◽  
R J Youle
Keyword(s):  
Retinoic Acid ◽  
Golgi Apparatus ◽  
Retinoic Acid Receptor ◽  
Receptor Activation ◽  
Marker Enzyme ◽  
Ricin A Chain ◽  
Acid Receptor ◽  
A Chain ◽  
Ricin A

All-trans retinoic acid can specifically increase receptor mediated intoxication of ricin A chain immunotoxins more than 10,000 times, whereas fluid phase endocytosis of ricin A chain alone or ricin A chain immunotoxins was not influenced by retinoic acid. The immunotoxin activation by retinoic acid does not require RNA or protein synthesis and is not a consequence of increased receptor binding of the immunotoxin. Vitamin D3 and thyroid hormone T3, that activate retinoic acid receptor (RAR) cognates, forming heterodimers with retinoid X receptor (RXR), do not affect the potency of immunotoxins. Among other retinoids tested, 13-cis retinoic acid, which binds neither RAR nor RXR, also increases the potency of the ricin A chain immunotoxin. Therefore, retinoic acid receptor activation does not appear to be necessary for immunotoxin activity. Retinoic acid potentiation of immunotoxins is prevented by brefeldin A (BFA) indicating that in the presence of retinoic acid, the immunotoxin is efficiently routed through the Golgi apparatus en route to the cytoplasm. Directly examining cells with a monoclonal antibody (Mab) against mannosidase II, a Golgi apparatus marker enzyme, demonstrates that the Golgi apparatus changes upon treatment with retinoic acid from a perinuclear network to a diffuse aggregate. Within 60 min after removal of retinoic acid the cell reassembles the perinuclear Golgi network indistinguishable with that of normal control cells. C6-NBD-ceramide, a vital stain for the Golgi apparatus, shows that retinoic acid prevents the fluorescent staining of the Golgi apparatus and eliminates fluorescence of C6-NBD-ceramide prestained Golgi apparatus. Electron microscopy of retinoic acid-treated cells demonstrates the specific absence of any normal looking Golgi apparatus and a perinuclear vacuolar structure very similar to that seen in monensin-treated cells. This vacuolization disappears after removal of the retinoic acid and a perinuclear Golgi stacking reappears. These results indicate that retinoic acid alters intracellular routing, probably through the Golgi apparatus, potentiating immunotoxin activity indepedently of new gene expression. Retinoic acid appears to be a new reagent to manipulate the Golgi apparatus and intracellular traffic. As retinoic acid and immunotoxins are both in clinical trials for cancer therapy, their combined activity in vivo would be interesting to examine.

Ligand-inducible retinoid X receptor-mediated protein: DNA interactions in the retinoic acid receptor β2 gene promoter in vivo

1998 ◽  
Vol 136 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Masato Ikeda ◽  
Remco A Spanjaard ◽  
Elizabeth W Noordhoek ◽  
Akio Kawaguchi ◽  
Toshimasa Onaya ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Gene Promoter ◽  
Retinoid X Receptor ◽  
Dna Interactions ◽  
Acid Receptor ◽  
Protein Dna Interactions ◽  
Retinoic Acid Receptor Β2
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