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PLAG1 like zinc finger 1 (PLAGL1) is an **imprinted zinc finger transcription factor** involved in transcriptional regulation of genes controlling cell cycle arrest, apoptosis, and cell growth suppression[1][2][3][4]. It acts as both a transcriptional activator and repressor by binding GC-rich regulatory regions and interacting with various co-activators and co-repressors. PLAGL1 is expressed primarily from the paternal allele due to imprinting and plays a key role in fetal development and metabolic homeostasis, especially in the endocrine pancreas (controlling insulin secretion)[1][3]. Loss or silencing (often through hypermethylation) of PLAGL1 is observed in several cancer types and impairs its tumor suppressor function, while overexpression due to epigenetic errors can cause 6q24-related transient neonatal diabetes mellitus[1][2][3][4]. No direct pharmacological inhibitors or activators are currently marketed, but the gene's expression status and methylation profile serve as disease biomarkers and potential points of therapeutic intervention[1][4].
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