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UCHL1 deubiquitinates NOX4. 11 / 11
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"These findings indicate that H2O2 levels regulated by <span class="match term0">UCH-L1</span> are necessary for cell invasion to occur and demonstrate that <span class="match term0">UCH-L1</span> promotes cell invasion by up-regulating H2O2 via deubiquitination of <span class="match term1">NOX4</span>"
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"Because H 2 O 2 generating activity of NOX4 is negatively modulated by ubiquitination and UCH-L1 promotes ROS induced cell invasion and migration in HeLa cells by deubiquitinating the NOX4 [13], we in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"We examined the deubiquitination of NOX4 by UCH-L1 in HUVECs control and HUVECs cells in which UCH-L1 was knocked down using siRNA."
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"Fig. 4 B shows that ubiquitination of NOX4 was markedly decreased by adding back of control UCH-L1 in UCH-L1-knocked down HUVECs."
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"Also, we demonstrated that UCH-L1 restores H 2 O 2 -gernerating activity of NOX4 by deubiquitinating NOX4."
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"We further investigated whether endogenous NOX4 is also deubiquitinated by UCH-L1 in B16F10 cells."
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"These immunoprecipitation studies confirm that UCH-L1 deubiquitinates NOX4 in HUVECs, and suggest that UCH-L1 is involved in ROS mediated angiogenesis in HUVECs by modulating NOX4 activity via deubiqu[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Immunoprecipitation studies confirmed that UCH-L1 deubiquitinates NOX4, suggesting that UCH-L1 might be involved in H 2 O 2 -mediated cell invasion by regulating the NOX4 activity through deubiquitination."
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"UCH-L1 restores H 2 O 2 -generating activity of NOX4 by deubiquitinating NOX4."
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"In the present study, we have shown that UCH-L1 deubiquitinates NOX4, thereby up-regulating its ability to generate H 2 O 2 and promoting the invasive potential of B16F10 cells both in vitro and in vivo."
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"We further showed that UCH-L1 increases ROS levels in HUVEC by deubiquitinating NOX4 in VEGF signaling."
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