EC Number   |
Application |
Reference |
|---|
    1.1.1.141 | drug development |
induction of 15-hydroxyprostaglandin dehydrogenase expression or utilization of 15-keto-PGE2 analogue may have therapeutic benefits for the treatment of endotoxin-associated liver inflammation/injury |
763614 |
| 1.1.1.141 | medicine |
15-hydroxyprostaglandin dehydrogenase hypomorphic mice show a decreased level of enzyme mRNA and activity in all tissues examined. Mice show spontaneous preterm labor in the absence of progesterone withdrawal, and the onset of labor is preceded by prematurely increased concentrations of prostaglandin E2 and F2alpha. The fetal genotype plays a role in birth timing |
688995 |
| 1.1.1.141 | medicine |
A140P is a naturally occuring mutation in patients with pulmonary hypertrophic osteoarthropathy. Homozygous individuals develop pulmonary hypertrophic osteoarthropathy secondary to chronically elevated prostaglandin E2 levels. Heterozygous relatives also show milder biochemical and clinical manifestations. Identification of an insertion-deletion mutation in 15-hydroxyprostaglandin dehydrogenase exon 3, this alters the open reading frame from codon 78, truncating the protein after ten altered amino acids, and of a homozygous 2-bp deletion within the duplicated dinucleotide CTCT at nucleotides 175 and 176. This alters the reading frame from residue 59 and truncates the HPGD protein at residue 65 after seven altered amino acids. Both of these predicted truncated proteins lack the entire PGE2-binding domain and cause primary hypertrophic osteoarthropathy |
689129 |
| 1.1.1.141 | medicine |
expression in nontumorigenic IEC-18 cells, with and without K-RasV12 and analysis of the ability of cells to form tumors in nu/nu mice. Transformed cells show increased 15-hydroxyprostaglandin dehydrogenase activity with decreased prostaglandin E2 and prostaglandin I2 levels, cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression and proliferation rates. Xenografts of cells expressing both the enzyme and K-RasV12 exhibit delayed tumor formation with negligible cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression and significantly decreased prostaglandin E2 levels. Tumors have decreased staining of the proliferative marker, Ki-67, and a significant increase in apoptosis in the central region of the tumor |
688932 |
| 1.1.1.141 | medicine |
in non-small-cell lung cancer cells, i.e. NSCLC cells, much lower expression of 15-hydroxyprostaglandin dehydrogenase in all histologic groups compared with healthy lung cell. Treatment with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib increases the expression of the enzyme in a subset of NSCLC lines |
685947 |
| 1.1.1.141 | medicine |
loss of 15-hydroxyprostaglandin expression in 65% of lung cancers. Enzyme acts as a tumor suppressor in lung cancer and is a direct downstream effector of hepatocyte nuclear factor 3beta |
685958 |
| 1.1.1.141 | medicine |
PGDH expression suppresses K-RasV12-mediated tumorigenesis in intestinal epithelial cells |
688932 |
| 1.1.1.141 | medicine |
thiazolidinediones rosiglitazone and pioglitazone upregulate expression of 15-hydroxyprostaglandin dehydrogenase, involving peroxisome proliferator-activated receptor gamma. Upregulation results in reduced production of prostaglandin E2 and finally inhibition of lung cancer growth |
689069 |
| 1.1.1.141 | medicine |
up-regulation of cyclooxygenase-2 expression by pro-inflammatory cytokines is accompanied by down-regluation of 15-hydroxyprostaglandin dehydrogenase expression. Over-expression of cyclooxygenase-2 but not -1 also attenuates 15-hydroxyprostaglandin dehydrogenase expression. Similarly, overexpression of 15-hydroxyprostaglandin dehydrogenase inhibits interleukin 1beta-induced cyclooxygenase-2 expression and results in apoptosis. The levels of 15-hydroxyprostaglandin dehydrogenase expression in transfected cells correlate positively with those of mesenchymal markers, and negatively with those of epithelial markers |
689843 |
