◀ Back to IL13
IL13 — IL13RA1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Dip Interaction:
IL13RA1
—
IL13
(direct interaction, surface plasmon resonance)
Lupardus et al., Structure 2010*
-
IRef Dip Interaction:
IL13RA1
—
IL13
(direct interaction, isothermal titration calorimetry)
Lupardus et al., Structure 2010*
-
IRef Dip Interaction:
IL13RA1
—
IL13
(direct interaction, cross-linking study)
Aman et al., J Biol Chem 1996*
-
IRef Hprd Interaction:
IL13RA1
—
IL13
(in vivo)
Oshima et al., J Biol Chem 2001*
-
IRef Innatedb Interaction:
IL13RA1
—
IL13
(unknown, -)
Miloux et al., FEBS Lett 1997
-
IRef Intact Interaction:
IL13RA1
—
IL13
(physical association, molecular sieving)
LaPorte et al., Cell 2008*
-
IRef Intact Interaction:
IL13RA1
—
IL13
(direct interaction, isothermal titration calorimetry)
LaPorte et al., Cell 2008*
-
IRef Intact Interaction:
Complex of 13 proteins
(direct interaction, x-ray crystallography)
LaPorte et al., Cell 2008*
-
IRef Ophid Interaction:
IL13RA1
—
IL13
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Myrtek et al., Immunology 2004
:
Whereas
IL-13 and IL-4
had inhibitory effects on
IL-13Ralpha1 expression on eosinophils, interferon-gamma, tumour necrosis factor-alpha, and, to the largest extent, transforming growth factor-beta, enhanced the expression of this receptor subunit
Finkelman et al., J Immunol 2005
(Bronchial Hyperreactivity) :
Although IL-4 signals through two receptors, IL-4R alpha/common gamma-chain ( gamma(c) ) and IL-4R
alpha/IL-13R alpha1 , and only the latter is also
activated by
IL-13 , IL-13 contributes more than IL-4 to goblet cell hyperplasia and airway hyperresponsiveness in murine asthma
Kasaian et al., Biochem Pharmacol 2008
(Asthma...) :
On B cells, monocytes, epithelial cells, and smooth muscle cells,
IL-13 acts through the
IL-13Ralpha1/IL-4Ralpha complex to directly induce activation responses that contribute to atopic disease