fig3

RET in breast cancer: pathogenic implications and mechanisms of drug resistance

Figure 3. Intracellular pathways, switched on by RET and receptor tyrosine kinase (RTK), leading to the activation of estrogen receptor (ER). The activation of RET and other RTKs by specific ligands and growth factors induces both the RAS/RAF/ERK pathways and the PI3K/AKT/mTOR pathways. Phosphorylation of ER can be mediated directly by ERK, AKT, mTOR, p38, p706SK and p90RSK, or other intracellular kinases. ER has five phosphorylation sites, three in the AF-1 domain and two in the AF-2 domain. Red arrows indicate the principal RET-dependent ER-phosphorylation site. Full and broken arrows indicate known and hypothetical interactions, respectively. This figure was created by Biorender.com

Cancer Drug Resistance
ISSN 2578-532X (Online)

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