ArticleJournal of molecular neuroscience : MN2017
In-depth Characterization of the Homodimerization Domain of the Transcription Factor THAP1 and Dystonia-Causing Mutations Therein.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Computational Identification of Milk Trait Regulation Through Transcription Factor Cooperation in Murciano-Granadina Goats.Biology · 2024Article
- Bioinformatic analysis of THAP9 transposase homolog: conserved regions, novel motifs.Current research in structural biology · 2024Article
- A pathogenic DYT-THAP1 dystonia mutation causes hypomyelination and loss of YY1 binding.Human molecular genetics · 2022Article
- DREAM represses distinct targets by cooperating with different THAP domain proteins.Cell reports · 2021Article
- THAP11 Functions as a Tumor Suppressor in Gastric Cancer through Regulating c-Myc Signaling Pathways.BioMed research international · 2020Article
- Article
- Classification of the human THAP protein family identifies an evolutionarily conserved coiled coil region.BMC structural biology · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
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Abstract
Mutations in the THAP1 gene encoding the transcription factor THAP1 have been shown to cause DYT6 dystonia. THAP1 contains a highly conserved THAP zinc finger at its N-terminal region which allows specific binding to its target sequences as well as a coiled-coil domain (amino acids 139-190) towards its C-terminus postulated as a protein-protein-binding motif. While several DYT6-causing mutations within the THAP domain were shown to decrease THAP1 activity in transcriptional regulation and DNA-binding, the role of mutations within the coiled-coil domain is rather unknown. Therefore, assigning a function to this domain may enable functional testing of mutations in this region. Notably, THAP1 and other THAP proteins form homodimers; however, the responsible domain has not been elucidated in detail. We show that the region of amino acids 139-185 is involved in formation of THAP1 homodimers by using yeast-two-hybrid, GST pull-down, and cross-linking assays. Surprisingly, all nine reported DYT6-causing missense mutations within this region had no effect on dimerization of THAP1 in GST pull-down and formaldehyde cross-linking assays. In conclusion, we demonstrated that a region of 47 amino acids is involved in THAP1 homodimerization but mutations in this region seem not to impair this mechanism.
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