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USP18 activates SLC7A11. 4 / 4
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"Likewise, USP18 knockdown inhibited cell viability, which was rescued by ectopic SLC7A11 expression (Fig. 5L and SI Appendix, Fig. S6L), suggesting the survival-promoting role of USP18 is mediated via up-regulating SLC7A11."
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"We propose that during breast carcinogenesis, decreased KCTD10 and increased USP18 would cause SLC7A11 accumulation to increase cystine uptake and consumption for the maintenance of rapid metabolism."
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"Thus, in contrast to KCTD10, USP18 promotes the survival of breast cancer cells by stabilizing SLC7A11 to suppress ferroptosis."
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"Upon cystine starvation, the levels of KCTD10 or USP18 are decreased or increased, respectively, to cause accumulation of SLC7A11, leading to enhanced cystine uptake/consumption and resistance to ferroptosis (Fig. 7L)."
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