Fig. 4: DHA inhibited the ubiquitination and degradation of NRF1 at the ER membrane. | Cell Death & Disease

Fig. 4: DHA inhibited the ubiquitination and degradation of NRF1 at the ER membrane.

From: NRF1 is upregulated by docosahexaenoic acid to ameliorate MASH through the inhibition of ER stress

Fig. 4: DHA inhibited the ubiquitination and degradation of NRF1 at the ER membrane.

A The half-life of NRF1 in HepG2 cells after DHA stimulation, as indicated by 10 μg/mL CHX treatment for various durations (n = 3 for each group). B Synthesis of NRF1 in HepG2 cells in response to stimulation with various fatty acids, as indicated by 10 μM MG132 treatment for 6 h. C, D Coimmunoprecipitation assay reflecting the interaction between NRF1-Flag and HA-FBW7 (C) or HA-HRD1 (D) in HepG2 cells treated with various fatty acids. E Ubiquitination of NRF1 in HepG2 cells overexpressing NRF1-Flag and HA-Ub upon DHA stimulation, as indicated by a coimmunoprecipitation assay. F NRF1 expression in HepG2 cells overexpressing wild-type NRF1 or mutant NRF1 deficient in amino acids 1–103 treated with DHA. G Coimmunoprecipitation assay indicating the interaction between NRF1-Flag and HA-DDI2, which were overexpressed in HepG2 cells stimulated with various fatty acids.

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