• KLF7 zinc fingers are essential for its regulatory control over NF-κB signaling and fatty acid β-oxidation genes.
• Deletion of zinc fingers alters NF-κB pathway activity in a cell-type-specific manner, with loss reducing activity in HeLa and EC109 cells but increasing it in Ishikawa cells.
• The ability of KLF7 to upregulate proinflammatory cytokines IL-6 and TNF-α is diminished upon zinc finger loss.
• These findings highlight the potential of targeting KLF7 zinc fingers for therapeutic intervention in inflammatory and metabolic diseases.
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