Abstract:IntroductionHeat shock protein 70.3 (Hsp70.3) expression is increased in response to cellular stress and plays a cytoprotective role, including a cardioprotective role in the heart against ischemia/reperfusion (I/R) injury. Recent work from our lab shows that Hsp70.3 expression following I/R is controlled through alternative polyadenylation (APA). Truncation of the 3′UTR removes potential regulatory sequences and is observed concomitant with upregulation of Hsp70.3 expression. Herein, we investigated the hypot… Show more
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