Gene interactions and pathways from curated databases and text-mining

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GJA1 — IL1A

Text-mined interactions from Literome

Tonon et al., J Bone Miner Res 2000 (Calcium Signaling) : IL-1 dependent up-regulation of Cx43 could be prevented by intracellular Ca2+ chelation but not by inhibitors of protein tyrosine kinases, suggesting a crucial role of cytosolic Ca2+ in regulating the expression of Cx43
Tonon et al., Biorheology 2002 : IL-1 dependent up-regulation of connexin 43 could be prevented by intracellular Ca2+ chelation, but not by inhibitors of protein tyrosine kinases, suggesting a crucial role of cytosolic Ca2+ in regulating the expression of connexin 43
Li et al., J Biol Chem 2011 (Cystitis) : Stimulation of BSMCs with IL1ß and TNFa increased connexin43 (Cx43) expression and function, which was associated with increased phosphorylation of vasodilator stimulated phosphoprotein
Baum et al., Am J Physiol Heart Circ Physiol 2012 (Arrhythmias, Cardiac...) : In vitro studies showed that IL-1ß caused loss of Cx43 and reduced coupling ... In conclusion, an increase of myofibroblasts in the infarcted heart causes heterogeneous Cx43 levels, possibly as a result of the release of IL-1ß and decreased cell-cell communication, which leads to conduction abnormalities following MI
Thota et al., Reprod Sci 2013 : Vitamin D also attenuated IL-1ß induced MCP-1, IL-6, connexin 43 , cyclooxygenase (COX)-2, and prostaglandin receptor expression ... Western analysis showed that vitamin D decreased MCP-1, TLR-4, and connexin 43 in the presence of LPS and decreased connexin 43 in the presence of IL-1ß
Negoro et al., Scientific reports 2013 (Disease Models, Animal...) : In urothelial cells, IL-1ß stimulation increased Cx43 expression, dye coupling, and p38 MAPK phosphorylation but not ERK1/2 phosphorylation ... SB203580 ( p38 MAPK inhibitor ) prevented IL-1ß induced Cx43 upregulation