To Browse through specific   lists, the search terms can   be prefixed with following   letters:
   d:  for diseases
   m: for molecules
   p:  for pathways
    c:  for cell lines
   v:  for interaction terms

*Search for genes, compounds, disease, cell/cell lines, organ, disease, pathway, process. (E.g Breast Neoplasms AND EGFR)

Modules Statistics Flexibility to integrate Publication and
Posters
Case Study Collaboration Testimonials Press Release
Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
139226AlbuterolSmall moleculeSmall moleculeInhibits expressionindirectTNFProteinHomo sapiens
In this article, we describe the results of studies designed to determine the extent to which IL-10 contributes to the suppression of TNF-alpha generation from LPS-stimulated human monocytes evoked by 8-bromo cyclic AMP (8-Br-cAMP), rolipram, salbutamol, and prostaglandin E2 (PGE2). / LPS evoked a time- and concentration-dependent generation of TNF-alpha (t1/2 = 4.5 h; EC50 = 273 pg/mL), which was inhibited by exogenous human recombinant (h) IL-10 (IC50 = 124 pg/mL), and by rolipram (EC50 = 420 nM), 8-Br-cAMP (EC50 = 77 (microM), PGE2 (EC50 = 15 nM) and salbutamol (EC50 = 20 nM).