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EGF — SLC9A1

Pathways - manually collected, often from reviews:

• NCI Pathway Database ErbB1 downstream signaling: NHE1 (SLC9A1) → EGFR/EGFR/EGF/EGF complex (EGFR-EGF) (modification, collaborate)
  Coaxum et al., Biochim Biophys Acta 2009*
  Evidence: physical interaction
• NCI Pathway Database ErbB1 downstream signaling: EGFR/EGFR/EGF/EGF complex (EGFR-EGF) → CaM/NHE1 complex (CALM2-SLC9A1) (modification, activates)
  Coaxum et al., Biochim Biophys Acta 2009*
  Evidence: physical interaction

Text-mined interactions from Literome

Mukhin et al., J Biol Chem 2004 : EGF receptor blockade attenuated ERK activation, but not NHE-1 activation by 5-HT and Ang II, suggesting that the EGF receptor and NHE-1 work in parallel to stimulate ERK activity in RASM cells, converging distal to the EGF receptor but at or above the level of Ras in the Ras-MEK-ERK pathway
Chiang et al., J Cell Physiol 2008 (Neoplasm Invasiveness...) : EGF upregulates Na+/H+ exchanger NHE1 by post-translational regulation that is important for cervical cancer cell invasiveness ... This study is to investigate the mechanisms by which epidermal growth factor (EGF) regulates NHE1 expression to promote cervical cancer cell invasiveness and the clinical significance in early-stage cervical cancer ... Image studies and immunoprecipitaion experiments suggest that EGF induced NHE1 translocation to the leading-edge lamellipodia, where NHE1 interacted with actin associated protein Ezrin, thereby remodeling cytoskeleton and stimulating cervical cancer cell migration ... In conclusion, EGF upregulates NHE1 by post-translational regulation that is important for cervical cancer cell invasiveness
Coaxum et al., Biochim Biophys Acta 2009 : Furthermore, pharmacological inhibitors of Janus kinase ( Jak2 ) and calmodulin (CaM) attenuated EGF induced NHE-1 activity ... 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
De Giusti et al., Hypertension 2011 : Epidermal growth factor was also able to increase reactive oxygen species production, and the epidermal growth factor induced activation of the NHE-1 was abrogated by the reactive oxygen species scavenger N-2-mercaptopropionyl glycine, indicating that reactive oxygen species are participating as signaling molecules in this mechanism