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"In addition, ACAT1 is a target for proteasomal degradation as USP19 was found to enhance cholesterol esterification through deubiquitinating and stabilizing ACAT1 in hepatocellular carcinoma cells [ 3[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Loss of either SOAT1 or USP19 dramatically attenuates cholesterol esterification and hepatocarcinogenesis in the p53-deficient mice fed with either normal chow diet (NCD) or high-cholesterol, high-fat diet (HCHFD)."

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"Also, worth investigating is whether USP19 inhibitors are promising drugs against tumors in general, or only some specific types of tumors, like liver cancers with p53 deletions/mutations that originate in a NAFLD background.In conclusion, this study shows that p53 deletion/mutation increases USP19, which in turn stabilizes SOAT1, increases cholesterol esterification and accelerates tumor progression (Figure 1)."