Gene interactions and pathways from curated databases and text-mining

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IL13RA2 — IL4

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: IL13RA2 → IL4 (directlyIncreases, IL4 Activity)
    Evidence: Figure 1. Pathways to MUC5AC expression in COPD

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Zheng et al., J Allergy Clin Immunol 2003 : These effects were not specific for IL-13, because transgenic IL-4 , IL-10, and IFN-gamma also stimulated IL-13Ralpha2 mRNA accumulation while stimulating-not altering and inhibiting-IL-13Ralpha1 mRNA accumulation, respectively
David et al., Oncogene 2003 : Finally, TNFalpha was shown to potentiate IL-4/IL-13 induced IL-13Ralpha2 promoter activity when the same reporter construct was studied in stably but not in transiently transfected cells ... These results suggest that the synergistic effect of TNFalpha on IL-4/IL-13 induced IL-13Ralpha2 expression is dependent upon chromatin re-modeling events
Wongpiyabovorn et al., J Dermatol Sci 2003 (Dermatitis, Atopic...) : In contrast, IL-13Ralpha2 mRNA expression was up-regulated by IFN-gamma plus IL-4
Yasunaga et al., Cytokine 2003 (Asthma...) : Either IL-4 or IL-13 induced intracellular expression of IL-13Ralpha2 in BECs, which was STAT6 dependent and required de novo protein synthesis
Andrews et al., J Allergy Clin Immunol 2006 : However, we found that the transmembrane form of IL-13Ralpha2 could attenuate both IL-13 and IL-4 responses, even though the response to TNF-alpha was unaffected
Morimoto et al., J Immunol 2009 (Strongylida Infections) : An infection induced up-regulation of IL-13Ralpha2 gene expression was confined to smooth muscle and was dependent on STAT6 and IL-13, but not on IL-4