Abstract
Receptor tyrosine kinase (RTK) signaling promotes tumor cell proliferation and resistance to ionizing radiation. Inhibition of RTK post-translational modifications such as N-linked glycosylation (NLG) reduce levels of over-expressed RTKs and sensitize tumor cells to radiation therapy. We therefore developed a high throughput screening (HTS) strategy to identify compounds that inhibit endoplasmic reticulum (ER) protein processing and thus block RTK function.
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