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EGF — TGFA

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of EGF-EGFR → TGFA (decreases)
  Evidence: HB-EGF and TGFA, although immunologically distinct from EGF, reportedly inhibit the binding of EGF to its own receptor

Text-mined interactions from Literome

Yang et al., Crit Rev Oncol Hematol 2001 (Neoplasms) : ABX-EGF binds EGFr with high affinity ( 5x10 ( -11 ) M ), blocks the binding of both EGF and transforming growth factor-alpha ( TGF-alpha ) to various EGFr expressing human carcinoma cell lines, and inhibits EGF dependent tumor cell activation, including EGFr tyrosine phosphorylation, increased extracellular acidification rate, and cell proliferation
Minter et al., Development 2002 : To determine whether steroid hormones directly modulate p53 activity, whole organ cultures of mammary glands were induced to proliferate using estrogen plus progesterone or epidermal growth factor plus transforming growth factor-alpha and p53 responses to gamma-irradiation were measured
Foon et al., Int J Radiat Oncol Biol Phys 2004 (Kidney Neoplasms...) : ABX-EGF binds EGFR and blocks receptor binding of EGF and transforming growth factor-alpha , inhibiting EGFR tyrosine phosphorylation and tumor cell activation
Yoshida et al., Jpn J Cancer Res 1990 (Carcinoma...) : We examined the effects of epidermal growth factor (EGF) and transforming growth factor-alpha ( TGF-alpha ) on EGF receptor (EGFR) phosphorylation and the expression of mRNAs for oncogenes, growth factors, their receptors and metalloproteinase genes by MKN-28 gastric carcinoma cells which express EGF, TGF-alpha and EGFR genes
Breyer et al., Am J Physiol 1990 : Kinetic studies ( 0 degrees C ) revealed an association t1/2 of 20.7 min and a dissociation t1/2 of 27 min. Competition studies revealed that 125I-EGF binding was inhibited by unlabeled EGF or its homologue transforming growth factor-alpha , but not by parathyroid hormone or insulin
Fischer et al., J Biol Chem 1994 : Even more marked, especially in the delta clones ( -90 % ), was the inhibition of cell transformation induced by autocrine stimulation with transforming growth factor alpha of the overexpressed epidermal growth factor receptors or by other growth factor receptors and oncogenes ( platelet derived growth factor/platelet derived growth factor receptor beta, HER2/neu, and v-erbB )
Plaut et al., J Dairy Sci 1993 : The gland has epidermal growth factor receptors, and epidermal growth factor or transforming growth factor-alpha can stimulate proliferation of mammary epithelial cells in vitro
Fan et al., J Biol Chem 1993 : Bivalent 225 mAb or monovalent 225 Fab ' inhibited transforming growth factor (TGF)-alpha induced EGF receptor tyrosine phosphorylation and cell proliferation
Li et al., Hum Reprod 1997 : Epidermal growth factor (EGF) , transforming growth factor alpha ( TGF alpha ) and insulin-like growth factor-I (IGF-I) stimulated NPC cell proliferation
Gulliford et al., Oncogene 1997 (Carcinoma, Squamous Cell) : Reduced ability of transforming growth factor-alpha to induce EGF receptor heterodimerization and downregulation suggests a mechanism of oncogenic synergy with ErbB2
Ramljak et al., Cancer Res 1998 (Helicobacter Infections...) : EGF and transforming growth factor-alpha were increased at the earliest stage, with a further increase in EGF in tumors