IndraLab

Statements


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"The adverse phenotypes observed in 2-week TAC-CR-CYLD mice were reminiscent of those in CR-mTOR KO mice, including inhibited p-p70S6K, accumulated autophagic vacuoles with undegraded contents, cardiomyocyte death, and cardiac dysfunction [ xref ], supporting the axis of CYLDmTORC1 inactivation–autolysosome efflux inhibition–cardiomyocyte death in PO-hearts."

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"Thus, except aforementioned K63 deubiquitination of mTOR and Rab7, the potential of TRIM28 or TRIMP37 and CYLD interaction in mTORC1 reactivation and suppressing autolysosome efflux in the heart deserves further investigation."