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This study discovered that the oncoprotein SRC is recruited and activated at the ER, triggering a cascade of pathways leading to the escape of the ER chaperones to the cell surface. At the cell surface, the chaperone protein GRP78 via interaction with CD109, suppresses TGF-b signaling.
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This page is a summary of: Endoplasmic reticulum stress activates SRC, relocating chaperones to the cell surface where GRP78/CD109 blocks TGF-β signaling, Proceedings of the National Academy of Sciences, April 2018, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.1714866115.
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