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• W1969016031 endingPage "390" @default.
• W1969016031 startingPage "381" @default.
• W1969016031 abstract "Abstract Mutations or deletions of the TRPS1 gene on human chromosome 8q.24.1 cause the tricho-rhino-phalangeal syndromes (TRPS), which are characterized by craniofacial and skeletal malformations. The gene encodes a transcription factor that functions as a repressor for GATA-mediated transcription. The activity of transcription factors is often controlled by posttranslational modifications. We show here that TRPS1 is SUMOylated at multiple sites, both in vivo and in vitro , through interaction with UBC9. Overexpression of wild-type UBC9 enhances TRPS1-mediated transcriptional repression. In contrast, a SUMOylation-deficient UBC9 mutant, which nevertheless still binds TRPS1, has no effect. Of the five potential TRPS1 SUMO-target sites, which were predicted based on a minimal SUMOylation consensus sequence (MCS), two are located within the C-terminal repression domain (RD) at lysine residues 1192 (termed S4) and 1201 (S5). S5 was identified as the major acceptor site within this region, and a point mutation of S5 strongly decreases TRPS1-RD-mediated transcriptional repression. Additional mutation of S4 results in abrogation of SUMOylation at the TRPS1-RD and almost complete loss of the repressive properties of TRPS1. These results identify SUMOylation at the TRPS1-RD as a major mechanism that regulates the function of TRPS1." @default.
• W1969016031 created "2016-06-24" @default.
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• W1969016031 creator A5055698670 @default.
• W1969016031 creator A5064965593 @default.
• W1969016031 date "2007-03-28" @default.
• W1969016031 modified "2023-10-16" @default.
• W1969016031 title "SUMOylation modulates transcriptional repression by TRPS1" @default.
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• W1969016031 doi "https://doi.org/10.1515/bc.2007.051" @default.
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