IndraLab

Statements


USP20 is phosphorylated on S132. 22 / 22
10 | 12

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"Phosphorylation of USP20 at Ser132 and Ser368 residues was detected through MS analysis (Figure xref )."

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"And the phosphorylation of USP20 at Ser132 and Ser368 requires the activation of ATR induced by DNA damage xref ."

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"USP20 phosphorylation at Ser132 and Ser368 enhanced its stability and thus conferred OXA and ferroptosis resistance of HCC cells (Figure  xref )."

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"Most importantly, DNA damage‐induced ATR activation is required for Ser132 and Ser368 phosphorylation of USP20."

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"USP20 phosphorylation at Ser132 and Ser368 enhances its stability and thus confers OXA and ferroptosis resistance of HCC cells."

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"Postprandial increases in insulin and glucose concentrations synergistically activated mTORC1 and phosphorylate USP20 at S132 and S134."

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"Postprandial increases in insulin and glucose levels stimulate mTORC1 to phosphorylate USP20 at S132 and S134; USP20 is recruited to the HMGCR complex and counteracts its degradation."

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"Specifically, feeding mice a high-sucrose, low-fat diet stimulated mTORC1 to phosphorylate USP20 at S132 and S134."

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"Elevated postprandial glucose and insulin levels stimulate mTORC1 to phosphorylate S132 and S134 in USP20."

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"Most importantly, DNA damage‐induced ATR activation was required for Ser132 and Ser368 phosphorylation of USP20."

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"The post-prandial increase in insulin and glucose concentration stimulates mTORC1 to phosphorylate USP20 at S132 and S134; USP20 is recruited to the HMGCR complex and antagonizes its degradation."

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"USP20 phosphorylation at Ser132 and Ser368 enhanced its stability and thus conferred OXA and ferroptosis resistance of HCC cells."