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"We further found that ectopic expression of USP38 also stabilized the HIF1α hydroxylation-deficient mutants, HIF1α (in which Pro 402 and 564, and Asp 803 were mutated to alanine) and HIF1α (in which Pro402 and 564 were mutated to alanine) (Fig. S5), indicating that USP38-mediated HIF1α stabilization is independent of PHD/VHL-mediated oxygen-dependent degradation of HIF1α."