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The **mesoderm-specific transcript homolog protein** (MEST) is encoded by the MEST gene, an imprinted gene expressed predominantly from the paternal allele in both humans and mice[3][5][6]. MEST belongs to the alpha/beta hydrolase superfamily, and while its precise enzymatic activity remains unknown, it has been linked to critical roles in embryonic development and adipose tissue biology[1][3][6]. MEST mRNA is upregulated during adipocyte differentiation and is highly expressed in white adipose tissue, particularly in the context of obesity, where it correlates with adipose tissue expansion and adipocyte size[1][4][7]. Knockout or silencing of MEST inhibits adipose tissue expansion, while overexpression increases adipocyte size and can induce trans-differentiation of preadipocytes to hepatocyte-like cells[1][5]. Loss of imprinting of the MEST gene has been associated with certain cancers, and MEST may serve as a molecular biomarker for adipogenic activity and fat mass deposition[3][4][7]. Despite its regulatory importance in adipose biology, MEST is not currently considered a direct therapeutic target such as a receptor, enzyme, or transporter; its value as a biomarker and its involvement in disease pathology are more prominent than any known therapeutic targeting[4][5][7].
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