IndraLab

Statements


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"Targets for miR-181b include heat shock protein A5 (HSPA5) and ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1), and expression of miR-181b in N2A cells repressed HSPA5 and UCHL1 and protected cells against OGD induced cell death."

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"As shown in Figure XREF_FIG D, UCHL1 shRNA 2 and 3 treatments reversed the increased cell death rate induced by cPKCgamma gene knockout in 1-hr OGD/24-hr R treated neurons (P < 0.001, n = 6 per group)."

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"In this study we demonstrated that Uch-L1 inhibition induces BACE1 up-regulation and increases neuronal and apoptotic cell death in control as well as in transgenic AD mouse model subjected to Bengal Rose, a light sensitive dye inducing that induces a cortical infarction through photo activation."

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"Inhibition of UCH-L1 activity induces the aggregation of Ub-proteins and enhances cell death in primary neurons."

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"Restoration of Uch-L1 Corrects the BACE1 Induction and Prevents Cell Death."

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"A previous study has shown that inhibition of UCH-L1 hydrolase activity induces the aggregation of ubiquitin-conjugated proteins and thus enhances cell death in primary neurons [23] ."

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"Expression of UCH-L1 was decreased by siRNA in both cell lines, resulting in increased cell death in H838 adenocarcinoma cells but not in the H157 squamous cell line."

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"UCHL1 mediated cell death can be attenuated by mitochondrial protein HTRA2 [XREF_BIBR], ATP13A2 regulates mitochondrial bioenergetics through macroautophagy [XREF_BIBR], VPS35 mediates vesicle transport between mitochondria and peroxisomes [XREF_BIBR], and EIF4G1 is involved in stress related protection of mitochondria [XREF_BIBR]."