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CALM3 — EGFR

Text-mined interactions from Literome

Belcheva et al., J Biol Chem 2001 (MAP Kinase Signaling System) : mu-Opioid receptor mediated ERK activation involves calmodulin dependent epidermal growth factor receptor transactivation
Li et al., Biochem J 2002 (Carcinoma, Squamous Cell) : Previous work from our laboratory has demonstrated that the Ca ( 2+ ) -calmodulin complex inhibits the intrinsic tyrosine kinase activity of the epidermal growth factor receptor (EGFR) , and that the receptor can be isolated by Ca ( 2+ ) -dependent calmodulin-affinity chromatography [ San José, Bengurija, Geller and Villalobo ( 1992 ) J. Biol. Chem. 267, 15237-15245 ]
Tebar et al., Mol Biol Cell 2002 (MAP Kinase Signaling System) : To examine the role of calmodulin in the regulation of EGFR , the effect of calmodulin antagonist, W-13, on the intracellular trafficking of EGFR and the MAPK signaling pathway was analyzed ... These data are consistent with the regulation of EGFR by calmodulin at several steps of the receptor signaling and trafficking pathways
Aifa et al., Cell Signal 2002 : Our results suggest that EGFR-JM is essential for epidermal growth factor (EGF) mediated calcium-calmodulin signalling and for signal integration between other signalling pathways
Bourguignon et al., J Biol Chem 2006 (Carcinoma, Squamous Cell...) : Overexpression of the LARG-PDZ domain also functions as a dominant negative mutant ( similar to the PLC/Ca2+-calmodulin dependent kinase II ( CaMKII ) and EGFR/MAPK inhibitor effects ) to block HA/CD44 mediated signaling events ( e.g. EGFR kinase activation, Ras/RhoA co-activation, Raf-ERK signaling, PLC epsilon mediated inositol 1,4,5-triphosphate production, intracellular Ca2+ mobilization, CaMKII activity, filamin phosphorylation, and filamin-actin binding ) and to abrogate tumor cell growth/migration
Deb et al., Am J Physiol Cell Physiol 2008 : Pregnancy upregulated nonubiquitous calmodulin kinase induces ligand independent EGFR degradation
Coaxum et al., Biochim Biophys Acta 2009 : The EGFR kinase inhibitor, AG1478, blocked activation of NHE-1, but did not block EGF induced phosphorylation of Jak2 or CaM ... These results suggest that EGF induces NHE-1 activity in podocytes through two pathways : ( 1 ) EGF -- > EGFR -- > Jak2 activation ( independent of EGFR tyrosine kinase activity ) -- > tyrosine phosphorylation of CaM -- > CaM binding to NHE-1 -- > conformational change of NHE-1 -- > activation of NHE-1 ; and ( 2 ) EGF -- > EGFR -- > EGFR kinase activation -- > association of CaM with NHE-1 ( independent of Jak2 ) -- > conformational change of NHE-1 -- > activation of NHE-1
Sánchez-González et al., FEBS J 2010 (Calcium Signaling) : Calmodulin mediated regulation of the epidermal growth factor receptor ... We also describe several mechanistic models that could account for the Ca ( 2+ ) /calmodulin mediated regulation of epidermal growth factor receptor activity
Li et al., J Biol Chem 2012 : Regulation of the ligand dependent activation of the epidermal growth factor receptor by calmodulin ... This occurred also in the presence of inhibitors of protein kinase C, CaM dependent protein kinase II and calcineurin, which are known Ca ( 2+ ) - and/or Ca ( 2+ ) /CaM dependent EGFR regulators, pointing to a direct effect of Ca ( 2+ ) /CaM on the receptor ... These results support the hypothesis that Ca ( 2+ ) /CaM regulates the EGFR activity by directly interacting with the CaM-BD of the receptor located at its cytosolic juxtamembrane region