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Statements


| 2

reach
"Moreover, the interaction of KDM4D and USP14/BRCC3 was increased with TRIM14 overexpression (SI Appendix, Fig. S5F), while TRIM14 deficiency significantly abrogated this interaction (Fig. 5D)."

reach
"Whether these TRIMs are in charge of KDM4D ubiquitination needs further investigation.Collectively, our data provide evidence for the autophagic control of epigenetic regulation in inflammation, as the TRIM14–USP14BRCC3 complex stabilizes KDM4D and prevents its autophagic degradation in DCs to mediate the pathogenesis of EAE (SI Appendix, Fig. S8)."