{'fraction_non_alphanumeric': 0.03139717425431711, 'fraction_numerical': 0.015698587127158554, 'mean_word_length': 6.203389830508475, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pontin52 and Reptin52 function as antagonistic regulators of β‐catenin signalling activity

In Wnt‐stimulated cells, β‐catenin becomes stabilized in the cytoplasm, enters the nucleus and interacts with HMG box transcription factors of the lymphoid‐enhancing factor‐1 (LEF‐1)/T‐cell factor (TCF) family, thereby stimulating the transcription of specific target genes. We recently identified Pontin52 as a nuclear protein interacting with β‐catenin and the TATA‐box binding protein (TBP), suggesting its involvement in regulating β‐catenin‐mediated transactivation. Here, we report the identification of Reptin52 as an interacting partner of Pontin52. Highly homologous to Pontin52, Reptin52 likewise binds β‐catenin and TBP. Using reporter gene assays, we show that the two proteins antagonistically influence the transactivation potential of the β‐catenin–TCF complex. Furthermore, we demonstrate the evolutionary conservation of this mechanism in Drosophila. dpontin and dreptin are essential genes that act antagonistically in the control of Wingless signalling in vivo. These results indicate that the opposite action of Pontin52 and Reptin52 on β‐catenin‐mediated transactivation constitutes an additional mechanism for the control of the canonical Wingless/Wnt pathway.