A short SUMOylation tag modulates transcription factor activity

This research demonstrates that a short peptide, composed of residues 24-55 of ZNF451, is sufficient to induce SUMOylation of target proteins, both in vitro and in human cells. Increased SUMOylation of the transcription factor p53 via fusion with the ZNF451 peptide inhibits its transcriptional activity, providing a proof of principle that targeted SUMOylation can be used to modulate the activity of targeted transcription factors.

本研究证实，一段由ZNF451第24至55位残基构成的短肽，足以在体外实验及人体细胞中诱导靶蛋白的小泛素样修饰（SUMOylation）。通过将该ZNF451短肽与转录因子p53融合，可提升其小泛素样修饰水平，进而抑制该转录因子的转录活性，这为靶向小泛素样修饰可用于调控靶转录因子活性提供了原理验证。