IndraLab

Statements



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"USP47 promotes apoptosis in rat myocardial cells after ischemia and reperfusion injury via NF-kappaB activation."

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"USP47 has also been described as an interaction partner for the ubiquitin E3 ligase complex, b-TrCP, with the authors of this study showing that silencing of USP47 expression inhibits cell survival and sensitises cells to chemotherapeutic agent-induced apoptosis [139] ."

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"USP47 induced apoptosis was potently counteracted by the NF-kappaB inhibitor, and cytoplasmic NF-kappaB was increased and nuclear NF-kappaB was decreased."

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"USP47 has also been described as an interaction partner for the ubiquitin E3 ligase complex, β-TrCP, with the authors of this study showing that silencing of USP47 expression inhibits cell survival and sensitises cells to chemotherapeutic agent-induced apoptosis [139]."

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"Downregulation of USP47 decreased apoptosis induced by ischemia/reperfusion injury, increased survivin and cytoplasmic NF-κB, and decreased cleaved caspase-3 and nuclear NF-κB. NF-κB inhibitors could effectively inhibit USP47-induced apoptosis, increase cytoplasmic NF-κB, and decrease nuclear NF-κB. Luciferase reporter genes showed that USP47 promoted NF-κB promoter activity."

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"USP47-deficient MEF cells isolated from a USP47 knockout mouse model revealed that USP47 knockout significantly increased the levels of ultraviolet-induced apoptosis (Peschiaroli et al., 2010)."