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The present data reveal that EGF and HB-EGF improve the proliferation of PCMOs by superactivating MEK/ERK signaling.
The results indicate that EGF increases SLPI expression.
Analysis of signaling pathway enrichment also showed that EGF signaling is active in recurrent AO.
The results showed that EGF signaling is highly associated with recurrent AO compared to other signaling pathways (Figure 3).
We found that EGF mutants with faster kinetic on-rates stimulate increased EGFR activation compared to wild-type EGF.
It is also possible, he says, that EGF was never that great a target to begin with.
Similar(9)
This demonstrates that EGF-HPPS specifically delivered its cargo (DiR-BOA) to target cells via EGFR-mediated endocytosis.
We found that EGF-conjugated dendrimers did not stimulate growth of EGFR-expressing cells at the selected concentration.
Few evidences suggested that EGF-R could modulate directly the immune system, but the consequences in response to bacteria injury remain unknown.
Lu et al. [48] proposed that EGF-induced AJ down-regulation is mediated via caveolae.
We have previously shown that EGF-induced MAPK activity is augmented in HeLa cells depleted of RKIP [1].
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