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Moreover, our data demonstrated that PRDX1-OE inhibited the activation of the JNK pathway by reducing the degradation of DOK3, while PRDX1 knockout led to increased JNK phosphorylation and decreased DOK3 protein levels upon stimulation with anti-mouse CD40 antibody, murine IL-21, and IL-4
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Monteith AJ, Miller JM, Maxwell CN, Chazin WJ, Skaar EP
however, the subsequent oxidation of 5-hmC into 5-fC and/or into 5-caC may only be driven by TET2 or TET3 [93]
