Epidermodysplasia verruciformis (EV) is an autosomal recessive dermatosis characterized by abnormal susceptibility to human papillomaviruses (HPVs) and a high rate of progression to squamous cell carcinoma on sun-exposed skin. EV is caused by mutations in either of two adjacent genes, EVER1 and EVER2, located on chromosome 17q25.3. Both of these genes encode integral membrane proteins that localize to the endoplasmic reticulum and are predicted to form transmembrane channels. Both EVER1 and EVER2 are members of the transmembrane channel-like (TMC) protein family. EVER1 possesses eight trans-membrane domains and two leucine zipper motifs. EVER1 and EVER2 form a complex and interact with the zinc transporter 1 (ZnT-1), suggesting that EVER1 and EVER2 act to regulate cellular zinc balance. At least four isoforms of EVER1 are known to exist. This EVER1 antibody does not cross-react with EVER2.

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