MEST encodes a member of the alpha/beta hydrolase superfamily. It is imprinted, exhibiting preferential expression from the paternal allele in fetal tissues, and isoform-specific imprinting in lymphocytes. The loss of imprinting of this gene has been linked to certain types of cancer and may be due to promotor switching. Mesoderm-specific transcript homolog protein may play a role in development. Alternatively spliced transcript variants encoding multiple isoforms have been identified for MEST. Pseudogenes of MEST are located on the short arm of chromosomes 3 and 4, and the long arm of chromosomes 6 and 15.
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