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This study characterizes Kaiso binding-site distribution in Caki-1 clear renal cancer cells using Kaiso-deficient cells as a negative control and compares the chromatin pattern with lymphoblastoid lines. The principal motifs are CGCG and CTGCNAT, with CpG islands showing wave-like methylation boundaries and enriched Kaiso presence. Identified target genes show methylation and transcription dependent on Kaiso expression.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/dissecting-the-kaiso-binding-profile-in-clear-renal-cancer-cells/337160/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/dissecting-the-kaiso-binding-profile-in-clear-renal-cancer-cells/337160.png","ImageObject",300,407,{"name":92,"@type":93},"Genevieve","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"Why is Kaiso’s in vivo binding profile of interest and what gap exists?","Question",{"text":113,"@type":114},"Kaiso is linked to clonal hematopoiesis, myelodysplastic syndrome, and tumorigenesis. However, consistent in vivo genomic binding-site data are lacking, and prior ChIP-seq results conflict with in vitro binding-site accumulation.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How does the study identify Kaiso genomic targets in clear renal cancer cells?",{"text":118,"@type":114},"The study uses Caki-1 kidney carcinoma cells and a derivative lacking the Kaiso gene as a model system. It characterizes the distribution of Kaiso binding sites and compares the chromatin pattern with lymphoblastoid cell lines.",{"name":120,"@type":111,"acceptedAnswer":121},"What DNA motifs and CpG island methylation features are associated with Kaiso binding?",{"text":122,"@type":114},"The principal binding motifs are CGCG and CTGCNAT, and 60% of binding sites contain both sequences. 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Epigenetics & Chromatin (2024) 17:38 [https://doi.org/10.1186/s13072-024-00565-3](https://doi.org/10.1186/s13072-024-00565-3)  \nEpigenetics & Chromatin  \n RESEARCH Open Access  \nDissecting the Kaiso binding profile in clear   renal cancer cells  \nAlexey Starshin1, Pavel Abramov1, Yaroslava Lobanova1, Fedor Sharko1, Galina Filonova1, Dmitry Kaluzhny3, Daria Kaplun 1, Igor Deyev4, Alexander Mazur1, Egor Prokhortchou1,2 and Svetlana Zhenilo1*  \nAbstract  \nBackground There has been a notable increase in interest in the transcriptional regulator Kaiso, which has been linked to the regulation of clonal hematopoiesis, myelodysplastic syndrome, and tumorigenesis. Nevertheless, there are no consistent data on the binding sites of Kaiso in vivo in the genome. Previous ChIP-seq analyses for Kaiso contradicted the accumulated data of Kaiso binding sites obtained in vitro. Here, we studied this discrepancy by characterizing the distribution profile of Kaiso binding sites in Caki-1 cells using Kaiso-deficient cells as a negative control, and compared its pattern on chromatin with that in lymphoblastoid cell lines.  \nResults We employed Caki-1 kidney carcinoma cells and their derivative, which lacks the Kaiso gene, as a model system to identify the genomic targets of Kaiso. The principal binding motifs for Kaiso are CGCG and CTGCNAT, with 60% of all binding sites containing both sequences. The significance of methyl-DNA binding activity was confirmed through examination of the genomic distribution of the E535A mutant variant of Kaiso, which cannot bind methylated DNA in vitro but is able to interact with CTGCNA sequences. Our findings indicate that Kaiso is present at CpG islands with a preference for methylated ones. We identified Kaiso target genes whose methylation and transcription are dependent on its expression. Furthermore, Kaiso binding sites are enriched at CpG islands, with partial methylation at the 5’and/or 3’ boundaries. We discovered CpG islands exhibiting wave-like methylation patterns, with Kaiso detected in the majority of these areas. Similar data were obtained in other cell lines.  \nConclusion The present study delineates the genomic distribution of Kaiso in cancer cells, confirming its role  \nas a factor with a complex mode of DNA binding and a strong association with CpG islands, particularly with methylated and eroded CpG islands, revealing a new potential Kaiso target gene—SQSTM1, involved in differentiation of acute myeloid leukemia cells. Furthermore, we discovered the existence of a new class of CpG islands characterized by wave-like DNA methylation.  \nKeywords DNA methylation, Methyl-DNA binding proteins, Kaiso, CpG islands erosion, SQSTM1  \narticle note = online  \n*Correspondence: Svetlana Zhenilo[szhenilo@gmail.com](szhenilo@gmail.com)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2024, corrected publication 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/licenses/by-nc-nd/4.0/](http://creativecommons.org/licenses","cbCairhQYlq6X1QO","https://ap.wps.com/l/cbCairhQYlq6X1QO","pdf",6295931,"English","# Background\n# Results\n# Conclusion\n# Introduction\n## DNA methylation and chromatin regulation\n## Kaiso as a methyl-DNA binding regulator\n## Kaiso protein domains and transcriptional roles","[{\"question\":\"Why is Kaiso’s in vivo binding profile of interest and what gap exists?\",\"answer\":\"Kaiso is linked to clonal hematopoiesis, myelodysplastic syndrome, and tumorigenesis. However, consistent in vivo genomic binding-site data are lacking, and prior ChIP-seq results conflict with in vitro binding-site accumulation.\"},{\"question\":\"How does the study identify Kaiso genomic targets in clear renal cancer cells?\",\"answer\":\"The study uses Caki-1 kidney carcinoma cells and a derivative lacking the Kaiso gene as a model system. It characterizes the distribution of Kaiso binding sites and compares the chromatin pattern with lymphoblastoid cell lines.\"},{\"question\":\"What DNA motifs and CpG island methylation features are associated with Kaiso binding?\",\"answer\":\"The principal binding motifs are CGCG and CTGCNAT, and 60% of binding sites contain both sequences. Kaiso is preferentially present at CpG islands with partial methylation near 5’ and/or 3’ boundaries, including CpG islands with wave-like methylation patterns.\"}]","Dissecting the Kaiso binding profile in clear renal cancer cells | PDF",1790017944]