EGF Target Analysis Report Summary
About the Target
Based on the provided context information, some key viewpoints about EGF can be extracted:
EGF binding to EGFR leads to a switch from a closed, inactive state to an open, active state [1].
Mutations in or near the EGF binding pocket can result in ligand-independent activation of EGFR and resistance to certain therapies [1].
circHBEGF can regulate the expression of EGFR and activate EGF signaling, leading to the upregulation of ECM gene expression [2].
EGF is involved in molecular crosstalk among signaling pathways such as hedgehog, BRAF/Ras/MAPK, Wnt, and Akt [3].
Anti-HER2 therapy can act through targeting EGF and its receptor, HER2, but resistance mechanisms can involve the activation of other signaling pathways [4].
EGF binding to EGFR triggers spatial rearrangement from monomers to dimers, higher order multimers, nanoscale clusters, clathrin-coated pits, and endosomes [5].
Upon EGF binding, EGFR undergoes auto-transphosphorylation and activates the Ras-MAPK pathway [5].
Chemical dimerizers can be used to trap EGFR dimers and study their signaling properties [5].
References:
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Based on the provided information, several key viewpoints can be extracted regarding EGF:
EGFR signaling in primary breast cancer is primarily associated with pro-growth and pro-survival pathways, whereas in metastatic breast cancer, STAT1 signaling is enhanced, supporting EGF-induced apoptosis [6].
Inhibition of the MEK/Erk signaling pathway using the drug Trametinib can bias EGFR signaling towards STAT1-mediated apoptosis [6].
Different levels of EGF stimulation can lead to distinct signaling pathways and outcomes. For example, EGF stimulation can lead to the upregulation of TSPAN8 expression, enhancing cell invasion and tumor metastasis [8].
The conformation of the JM coiled-coil region in EGFR can be influenced by the type of growth factor (EGF or TGF-alpha) bound to the extracellular domain (ECD) of the receptor [9].
EGF stimulation and hypoxia contribute to the transcriptional regulation of KPNA2, a gene involved in lung ADC cells. EGF upregulates KPNA2 and E2F1 expression while suppressing IRF1 expression [10].
These findings highlight the complex and diverse roles of EGF in different cell types and contexts, ranging from pro-growth signaling to apoptosis and transcriptional regulation.
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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the EGF target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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