Extended Data Fig. 7: STK38 is responsible for SCRN1 mediated GPX4 phosphorylation. | Nature Cancer

Extended Data Fig. 7: STK38 is responsible for SCRN1 mediated GPX4 phosphorylation.

From: SCRN1 confers hepatocellular carcinoma resistance to ferroptosis by stabilizing GPX4 via STK38-mediated phosphorylation

Extended Data Fig. 7: STK38 is responsible for SCRN1 mediated GPX4 phosphorylation.The alt text for this image may have been generated using AI.

a, Dot plot showing GPX4-interacting proteins by using mass spectrometry. b, c, GPX4-Flag expression in HEK293T (b) and Huh7 (c) cells transfected with increasing STK38-Myc. d, GPX4-Flag expression in HEK293T cells transfected with increasing RIOK1-Myc. e, Endogenous interaction between STK38 and GPX4 in Huh7 cells. f, The mRNA expression of GPX4 in HepG2 cells transfected with control or STK38 siRNA (n = 3 biological replicates). g, GPX4-Flag expression in HEK293T cells transfected with STK38-Myc and treated with Baf-A1. h, The interaction between GPX4-Flag and LAMP2A in HEK293T cells transfected with STK38-Myc or control plasmid and treated with staurosporine or not. i, WT or S45A mutated GPX4 expression in HEK293T cells transfected with STK38-Myc. j-m, Establishment of stably STK38 KO HepG2 (j), Huh7 (k), HT1080 (l) and NIH3T3 (m) cells. n-s, Percentage of cell death (n, p, r) and C11-BODIPY fluorescence (o, q, s) of WT and STK38 KO Huh7, HT1080 and NIH3T3 cells treated with indicated FINs (n = 3 biological replicates). Data shown are representative of three independent experiments with similar results (b-e, g-m). Data presented as mean ± s.d. of three independent experiments and statistical significance was determined by two-tailed unpaired Student’s t-test (f, n-s).

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