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
23171TNFProteinHomo sapiens-eIncreases expressionindirectCCL20RNAHomo sapiens
The expression of MIP-3alpha was upregulated by infection with Actinobacillus actinomycetemcomitans and by stimulation with lipopolysaccharide and TNF-alpha.
Disease
115496CCL20ProteinHomo sapiensIncreases mobilizationindirectCalciumSmall moleculeSmall molecule
In contrast to other chemokines, including MCP-1 and IL-8, the natural processing did not affect the calcium-mobilizing capacity of LARC/MIP-3alpha through its receptor CCR6.
Regulator
115498CCL20ProteinHomo sapiensBinddirectCCR6ProteinHomo sapiens
In contrast to other chemokines, including MCP-1 and IL-8, the natural processing did not affect the calcium-mobilizing capacity of LARC/MIP-3alpha through its receptor CCR6.
192711NF-kappa-BMulti subunitHomo sapiens-eIncreases expressiondirectCCL20ProteinHomo sapiens-e
To investigate whether PEDF also modulates gene expression in astrocytes, we employed the use of RT-PCR to analyze the gene expression of certain pro-inflammatory genes and found that genes such as IL-1 beta, IL-6, TNF-alpha, MIP1 alpha, and MIP3 alpha were induced in PEDF-treated cultured neonatal astrocytes, but not in adult astrocytes. / These results suggest that the induction of pro-inflammatory genes is mediated via activation of NF-kappa B, AP-1, and CREB in neonatal astrocytes.