IndraLab

Statements


USP10 activates CH. 5 / 5
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"In contrast, cardiac overexpression of USP10 protected against pressure overload induced maladaptive CH."

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"Taken together, these results show that USP10 deficiency promotes pressure overload induced CH."

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"Taken together, these data indicate that the activation of the Akt/GSK3beta/mTOR/p70-S6K signaling pathways appears to be essential for USP10 mediated CH."

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"Our observations indicate that USP10 deficiency promotes pressure overload induced CH and alleviated Ang II induced cardiomyocyte enlargement, accompanied by significant decreases in the expression of the fetal genes Anp, Bnp, and Myh7, and vice versa."

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"Because key regulators of CH such as p53, AMPK, and TRAF6 have been reported as downstream targets of USP10, 20, 21 we first evaluated the potential involvement of these target proteins in the CH pathogenesis induced by USP10 deficiency."