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
232053ERBB2ProteinHomo sapiens-eIncreases expressionindirectTnfaip2ProteinMus musculus
ERBB2 amplification and overexpression have been found in a number of human cancers, including breast, ovary and kidney carcinoma. / The differential gene expression profile of ERBB2-transfected and wild-type mouse fibroblasts was monitored employing DNA microarrays. Regulated expression of selected genes was verified by RT-PCR and validated by Western blot analysis. / ERBB2 overexpression suppresses the transcription of antiangiogenic factors (e.g., Sparc, Timp3, Serpinf1) but induces expression of angiogenic factors (e.g., Klf5, Tnfaip2, Sema3c).
Disease
232089TNFProteinHomo sapiens-eIncreases expressionindirectTNFAIP2RNAHomo sapiens
We utilized cDNA representational difference analysis to identify the genes in which expression is induced by the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta in primary human bronchial epithelial cells and hence are relevant to airway inflammation. Hybridization of the subtraction product to arrayed cDNAs indicated that known tumor necrosis factor-alpha- and interleukin-1beta-inducible genes such as B94, Zfp36, and regulated on activation normal T cell expressed and secreted were represented, confirming the success of the subtraction experiment.
232091IL1BProteinHomo sapiens-eIncreases expressionindirectTNFAIP2RNAHomo sapiens
We utilized cDNA representational difference analysis to identify the genes in which expression is induced by the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta in primary human bronchial epithelial cells and hence are relevant to airway inflammation. Hybridization of the subtraction product to arrayed cDNAs indicated that known tumor necrosis factor-alpha- and interleukin-1beta-inducible genes such as B94, Zfp36, and regulated on activation normal T cell expressed and secreted were represented, confirming the success of the subtraction experiment.