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USP38 activates Hypoxia. 11 / 11
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"Furthermore, overexpression of USP38 enhanced the expression of hypoxia-inducible genes under hypoxia (Fig. 1C)."
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"To determine whether the screened USP38 specifically enhanced hypoxia signaling, we selected two additional USPs, USP53 and USP25, for validation."
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"In wild-type H1299 cells, overexpression of USP38 significantly enhanced hypoxia-stimulated expression of BNIP3 and VEGFA, but not in HIF1β-deficient H1299 cells (Fig. 1K)."
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"Taken together, these data suggest that USP38 enhances hypoxia signaling."
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"These data suggest that USP38 may enhance hypoxia signaling to influence cellular ROS and subsequent cell apoptosis dependent on HIF1α."
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"Although we provide evidence to support that USP38 can enhance hypoxia signaling by stabilizing HIF1α, the physiological relevance of this modulation is still largely unknown due to the lack of animal models."
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"Further investigation of the role of USP38 in modulating hypoxia signaling in vivo will provide insight into the physiological function of USP38 and the underlying molecular mechanisms."
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"USP38 promoted hypoxia-responsive gene expression under hypoxia."
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"We found that overexpression of USP38 increased hypoxia-responsive gene expression, but knockout of USP38 suppressed hypoxia-responsive gene expression under hypoxia."
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"USP38 enhances hypoxia signaling."
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"Overexpression of USP38 also enhanced CoCl -stimulated expression of hypoxia-inducible genes (Fig. 1B)."
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