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)

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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
66116Hydrogen peroxideSmall moleculeSmall moleculeIncreases activityindirectCASP3ProteinHomo sapiens-e
The membrane-permeable cGMP analog dibutyryl-cGMP attenuated the H(2)O(2)-induced decrease in cell viability, DNA ladder formation, nuclear condensation, reduction of the mitochondrial membrane potential, cytochrome c release from mitochondria, and caspase-3 activation in cultured astrocytes. / The PTP inhibitors cyclosporin A and bongkrekic acid prevented the H(2)O(2)-induced decrease in cell viability and caspase-3 activation.
Regulator
87378Hydrogen peroxideSmall moleculeSmall moleculeIncreases activityindirectMAP3K5ProteinHomo sapiens-e
Treatment of cells with N-acetyl-L-cysteine also inhibited serum withdrawal-, TNF-alpha- and hydrogen peroxide-induced activation of ASK1 as well as apoptosis.
Regulator
164872APPProteinHomo sapiensIncreases levelindirectHydrogen peroxideSmall moleculeSmall molecule
In Alzheimer's disease (AD), amyloid beta-peptide (A beta) fibrils accumulate in plaques which are associated with degenerating neurons. / We now report that bFGF can protect cultured hippocampal neurons against A beta25-35 toxicity by a mechanism that involves suppression of reactive oxygen species (ROS) accumulation and maintenance of Na+/K+-ATPase activity. A beta25-35 induced lipid peroxidation, accumulation of H2O2, mitochondrial ROS accumulation, and a decrease in mitochondrial transmembrane potential; each of these effects of A beta25-35 was abrogated in cultures pre-treated with bFGF.
Disease
Regulator