{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZNF148 (also known as ZBP‐89) is a multifunctional Krüppel‐type zinc finger transcription factor that exerts its effects by binding GC‐rich promoter elements and by interacting with other key regulators. In various developmental and differentiation contexts—including erythroid and megakaryocytic lineages, intestinal cells, neural precursors, and even myocytes—ZNF148 modulates gene expression through cooperative interactions with factors such as GATA‐1, FOG‐1, NF‐Y, and Sp family members. Its activity is further fine‐tuned by post‐translational modifications (for example, sumoylation) that alter cooperation with other activators, thereby influencing the expression of lineage‐specific targets such as globin genes, intestinal alkaline phosphatase, SOX18, and insulin receptor substrate 2."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of tumor biology, ZNF148 has been shown to influence cell fate by promoting growth arrest and apoptosis. It can stabilize or cooperate with p53 and upregulate cell cycle inhibitors like p21 while concurrently repressing pro‐senescence genes (for example, p16^INK4a) through epigenetic mechanisms that involve the recruitment of histone deacetylases and DNA methyltransferases. Such actions lead to the induction of apoptosis via the mitochondrial and JNK pathways, modulation of anti‐apoptotic factors (such as Bcl-xL and Mcl-1) and pro-apoptotic regulators like Bak and Pdcd4, and even the regulation of telomerase (by affecting TERT expression). Collectively, these tumor‐suppressive activities help limit neoplastic transformation and progression in cancers of the gastrointestinal tract, liver, and kidney."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, ZNF148 impacts a broad range of physiological and pathological processes beyond differentiation and tumor suppression. It participates in inflammatory pathways—as evidenced by its regulation by microRNAs in rheumatoid arthritis and its involvement in positive feedback loops with long noncoding RNAs during diabetic wound healing. In metabolic regulation, suppression of ZNF148 in pancreatic β cells enhances insulin secretion, and it modulates growth hormone receptor expression in response to fatty acids. Genetic studies further implicate aberrations in ZNF148 in intellectual disability syndromes and suggest roles in viral replication processes, such as in hepatitis B. Additional functions include promoting or restraining invasive behavior in cancers like colorectal and gastrointestinal stromal tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Heiyoung Park, C Simon Shelley, M Amin Arnaout "}, {"type": "b", "children": [{"type": "t", "text": "The zinc finger transcription factor ZBP-89 is a repressor of the human beta 2-integrin CD11b gene."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Blood (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1182/blood-2002-03-0680"}], "href": "https://doi.org/10.1182/blood-2002-03-0680"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12393719"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12393719"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "George G Chen, Juanita L Merchant, Paul B S Lai, et al. 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