enhanced activity and expression of RALDHs in liver of high-fat diet rats. High-fat diet feeding significantly up-regulates cytosolic RALDHs activity, 1.7fold and 2fold in the presence of NAD+ and NADP+, respectively
ERK and p38 MAPK inhibitors PD98059 and SB203580 suppress GM-CSF-induced nuclear translocation of Sp1 and Aldh1a2 expression. CpG methylation in the Aldh1a2 promoter region inhibits Sp1-dependent Aldh1a2 promoter activation. Aldh1a2 transcription silencing by CpG methylation of the promoter region is not due to direct interference with Sp1 binding to the promoter region
granulocyte-macrophage colony-stimulating factor (GMCSF) potently induces RALDH2 expression in dendritic cells in an retinoic acid-dependent manner, and retinoic acid alone weakly induces the expression. Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells
high retinoic acid levels inhibit Raldh1 gene expression by sequestering CCAAT/enhancer binding protein beta through its interaction to GADD153. A decrease in Raldh1 mRNA levels in the aryl hydrocarbon receptor-null liver relative to wild type mouse liver is observed
inflammation reduces ALDH1A1 mRNA in whole liver regardless of the level of vitamin A in the diet, while treatment with retinal reduces ALDH1A1 expression only in chow-fed rats. Acute inflammation rapidly downregulates ALDH1A1 expression in whole liver
levels of RALDH1 gene expression and protein production markedly decrease after 1-week treatment with 17beta-estradiol in male rats. Treatment of isolated anterior pituitary cells with 17beta-estradiol (0.00001-10 nM) decreases expression of RALDH1 mRNA in a dose-dependent manner (about 55% RALDH1 mRNA level remaining 6 h after treatment with 10 nM 17beta-estradiol). 17beta-Estradiol-induced suppression of RALDH1 expression is completely blocked by the estrogen receptor antagonist ICI 182, 780. The ERalpha-selective agonist propylpyrazole triol (10 nM) mimicks the effect of 17beta-estradiol on RALDH1 expression, but the ERbeta-selective agonist diarylpropionitrile (10 nM) does not
obesity and insulin resistance are associated with overexpression of retinaldehyde dehydrogenase 1. High-fat-diet-feeding significantly induces the activity and expression of RALDH1 protein
enhanced activity and expression of RALDHs in liver of high-fat diet rats. High-fat diet feeding significantly up-regulates cytosolic RALDHs activity, 1.7fold and 2fold in the presence of NAD+ and NADP+, respectively
enhanced activity and expression of RALDHs in liver of high-fat diet rats. High-fat diet feeding significantly up-regulates cytosolic RALDHs activity, 1.7fold and 2fold in the presence of NAD+ and NADP+, respectively
ERK and p38 MAPK inhibitors PD98059 and SB203580 suppress GM-CSF-induced nuclear translocation of Sp1 and Aldh1a2 expression. CpG methylation in the Aldh1a2 promoter region inhibits Sp1-dependent Aldh1a2 promoter activation. Aldh1a2 transcription silencing by CpG methylation of the promoter region is not due to direct interference with Sp1 binding to the promoter region
ERK and p38 MAPK inhibitors PD98059 and SB203580 suppress GM-CSF-induced nuclear translocation of Sp1 and Aldh1a2 expression. CpG methylation in the Aldh1a2 promoter region inhibits Sp1-dependent Aldh1a2 promoter activation. Aldh1a2 transcription silencing by CpG methylation of the promoter region is not due to direct interference with Sp1 binding to the promoter region
granulocyte-macrophage colony-stimulating factor (GMCSF) potently induces RALDH2 expression in dendritic cells in an retinoic acid-dependent manner, and retinoic acid alone weakly induces the expression. Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells
granulocyte-macrophage colony-stimulating factor (GMCSF) potently induces RALDH2 expression in dendritic cells in an retinoic acid-dependent manner, and retinoic acid alone weakly induces the expression. Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells