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The proposed therapeutic mechanism involves the down-regulation of c-Jun-N-terminal kinase (JNK) by inducing Gadd45-beta activity, which ultimately disrupts a mechanism of mitochondrial damage

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In-utero exposure to HT-2 toxin affects meiotic progression and early oogenesis in foetal oocytes by increasing oxidative stress

This competitive process plays a crucial role in regulating antitumor immunity

A Gold Standard-Derived Modular Barcoding Approach to Cancer Transcriptomics

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