{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZBTB33 (also known as Kaiso) is a unique POZ‐zinc finger transcription factor that mediates dual‐mode DNA binding. It recognizes both a sequence‐specific Kaiso binding site (KBS) and methylated CpG dinucleotides, thereby modulating target gene transcription. Structural and functional studies have demonstrated that Kaiso’s DNA recognition requires not only its three zinc finger domains but also additional regions that aid in nuclear import and stabilization of its DNA‐binding conformation. This multimodal binding ability underpins its role as a transcriptional regulator in normal development and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nKaiso’s function is tightly linked to its subcellular localization and its dynamic interaction with adhesion‐associated partners such as p120‑catenin. Through binding p120‑catenin, Kaiso’s nuclear entry, retention, and possibly its release from repressive complexes are modulated, thereby influencing the transcription of genes involved in cell adhesion and chromatin regulation. In some studies, Kaiso has also been shown to interact with insulator proteins like CTCF, suggesting a broader role in organizing chromatin domains and genomic imprinting. These interactions help explain context‐dependent functional outcomes and variations in Kaiso localization observed in normal and cancerous tissues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn its role as a transcriptional repressor, Kaiso directly occupies the promoters of genes crucial for cell cycle progression, EMT, and oncogenic signaling. By binding to methylated promoters or nearby KBS elements, it regulates the expression of targets such as cyclin D1, matrix metalloproteinases, and E-cadherin, thereby influencing cellular proliferation and differentiation. Epigenetic regulation by Kaiso is evident from its ability to sense promoter methylation and impose silencing, which may be reversed by agents that alter DNA methylation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in transcriptional repression, Kaiso actively modulates oncogenic pathways. It has been implicated in regulating epithelial–mesenchymal transition and cell motility, with alterations in its expression or localization correlating with aggressive tumor phenotypes in cancers including prostate, colon, and breast. Moreover, Kaiso influences miRNA expression and interfaces with signaling cascades such as Wnt/β‑catenin, thereby fine‐tuning the balance between proliferation and invasion. These findings underscore Kaiso’s importance as a molecular switch in the regulation of genes critical for cancer progression and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nKaiso also plays an essential role in mediating cellular stress responses. In the context of genotoxic stress, it contributes to p53 acetylation and enhances transcription of pro‑apoptotic genes, thereby ensuring an appropriate DNA damage response. Such regulatory crosstalk not only influences tumor cell survival but also has potential implications for therapeutic responses, as seen in studies linking Kaiso modulation to altered sensitivity to chemotherapy and glucocorticoids. Furthermore, recent work indicates that Kaiso’s modulation of these pathways may determine cell fate decisions during tumor progression and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "32", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jyothisri Kondapalli, Annette S Flozak, Maria Luiza C Albuquerque "}, {"type": "b", "children": [{"type": "t", "text": "Laminar shear stress differentially modulates gene expression of p120 catenin, Kaiso transcription factor, and vascular endothelial cadherin in human coronary artery endothelial cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M306057200"}], "href": "https://doi.org/10.1074/jbc.M306057200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "14699141"}], "href": "https://pubmed.ncbi.nlm.nih.gov/14699141"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Kevin F Kelly, Abena A Otchere, Monica Graham, et al. 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