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Statements

TRIM21 binds USP28. 10 / 10
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"Our study illustrates a cardiomyocyte-specific USP28-TRIM21 axis in regulating hypertrophic cardiomyopathy and indicates USP28 as a pharmacological target for cardiac hypertrophy."
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"USP28 binds TRIM21 to regulate deubiquitinated modification and stability of TRIM21."
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"We then confirmed the endogenous interaction between USP28 and TRIM21 in Ang II-induced HL-1 and heart tissues using co-IP assay (Fig. xref C)."
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"Subsequently, the ability of USP28-C171A to maintaining the protein stability of TRIM21 was also decreased, compared with wildtype USP28 (Fig. xref J), although USP28-C171A still bound to TRIM21 ( xref F)."
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"Taken together, USP28 binds to TRIM21 and regulates K48-linked deubiquitination and stability of TRIM21 via its active site C171 (Fig. xref K)."
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"Therefore, the role of USP28-TRIM21 axis in Ang II-induced oxidative stress was examined."
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"We then have investigated the binding of USP28 and TRIM21 and the maintenance of TRIM21 stabilization by USP28 via K48-linked deubiquitination."
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"Apart from the USP28-TRIM21 interaction, USP28 has been reported to deubiquitinate some other substrate proteins xref , such as Cyclin E1 xref and NICD1 xref ."
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"Given TRIM21 is not feasible as a therapeutic target for cardiac hypertrophy, due to its widespread expression in multi-organs, the cardiomyocyte-specific USP28-TRIM21 axis may avoid the potential and systemic side-effects induced by targeting TRIM21 alone, suggesting that targeting USP28 is a more specific strategy for cardiac hypertrophy therapy."
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"Conclusion: Our study illustrates a cardiomyocyte-specific USP28-TRIM21 axis in regulating hypertrophic cardiomyopathy and presents USP28 as a potential target for the treatment of cardiac hypertrophy."
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