IndraLab

"In the present study, there are several novel findings regarding UCH-L1 as a negative regulator of maladaptive cardiac remodeling and dysfunction as follows : (i) UCH-L1 expression is enhanced in cardiac myocytes and fibroblasts during the earlier stage of cardiac adaptive hypertrophy and declined in the process of maladaptive responses to the sustained hemodynamic stress; (ii) UCH-L1 inhibits cardiac fibroblast proliferation via suppressing PDGF and PDGFRbeta signaling; (iii) UCH-L1 preferentially enhances PDGF-BB-induced suppression autophagic clearance of p21 WAF1 and Cip1 proteins in cardiac fibroblasts."

"Of interest, overexpression of UCH-L1 enhanced the PDGF-BB-induced posttranscriptional upregulation of p21 WAF1 and Cip1 protein in cardiac fibroblasts (XREF_FIG), suggesting that UCH-L1 inhibits cardiac fibroblast proliferation via posttranscriptional enhancing the expression of p21 WAF1 and Cip1 to suppress the transition of G1 to S phase."

"UCH-L1 enhances PDGF-BB-induced upregulation of p21 WAF1 and Cip1 proteins via suppressing autophagic clearance of p21 WAF1 and Cip1 independent of ubiquitin-proteasomal system (UPS)-mediated protein degradation."

"To explore the underlying mechanism by which UCH-L1 enhances PDGF-BB-induced posttranscriptional upregulation of p21 WAF1 and Cip1, we determined a potential role of UCH-L1 in regulating p21 clearance by UPS and autophagy, two major pathways in the posttranscriptional control of protein levels XREF_BIBR."

"To explore the underlying mechanism by which UCH-L1 enhances PDGF-BB-induced posttranscriptional upregulation of p21 WAF1 and Cip1, we determined a potential role of UCH-L1 in regulating p21 clearance by UPS and autophagy, two major pathways in the posttranscriptional control of protein levels XREF_BIBR."

"In the present study, there are several novel findings regarding UCH-L1 as a negative regulator of maladaptive cardiac remodeling and dysfunction as follows : (i) UCH-L1 expression is enhanced in cardiac myocytes and fibroblasts during the earlier stage of cardiac adaptive hypertrophy and declined in the process of maladaptive responses to the sustained hemodynamic stress; (ii) UCH-L1 inhibits cardiac fibroblast proliferation via suppressing PDGF and PDGFRbeta signaling; (iii) UCH-L1 preferentially enhances PDGF-BB-induced suppression autophagic clearance of p21 WAF1 and Cip1 proteins in cardiac fibroblasts."

"UCH-L1 enhances PDGF-BB-induced upregulation of p21 WAF1 and Cip1 proteins via suppressing autophagic clearance of p21 WAF1 and Cip1 independent of ubiquitin-proteasomal system (UPS)-mediated protein degradation."

"Of interest, overexpression of UCH-L1 enhanced the PDGF-BB-induced posttranscriptional upregulation of p21 WAF1 and Cip1 protein in cardiac fibroblasts (XREF_FIG), suggesting that UCH-L1 inhibits cardiac fibroblast proliferation via posttranscriptional enhancing the expression of p21 WAF1 and Cip1 to suppress the transition of G1 to S phase."