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Review
. 2016 Apr;33(2):75-80.
doi: 10.5114/ada.2016.59145. Epub 2016 May 16.

The EVER genes - the genetic etiology of carcinogenesis in epidermodysplasia verruciformis and a possible role in non-epidermodysplasia verruciformis patients

Affiliations
Review

The EVER genes - the genetic etiology of carcinogenesis in epidermodysplasia verruciformis and a possible role in non-epidermodysplasia verruciformis patients

Agnieszka Kalińska-Bienias et al. Postepy Dermatol Alergol. 2016 Apr.

Abstract

In recent years, the two adjacent novel EVER1 and EVER2 genes have been identified, whose mutations are responsible for the development of epidermodysplasia verruciformis (EV). Epidermodysplasia verruciformis is a rare, autosomal recessive genodermatosis associated with increased risk of skin carcinoma. Up to now 7 mutations in the EVER1 gene and 5 mutations in the EVER2 gene have been identified only in EV. It was also determined that the EVER genes belong to a novel gene family, the transmembrane channel-like (TMC) family, and are responsible for properly functioning zinc homeostasis. These observations have given new insights into EV pathogenesis.

Keywords: EVER genes and proteins; carcinogenesis; epidermodysplasia verruciformis.

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Figures

Figure 1
Figure 1
Mechanism of action of EVER proteins in keratinocytes: A – infection of keratinocytes by genital HPV (HPV16) leads to synthesis of E5 protein and inhibition of the ZnT-1/EVER complex, which allows viral replication in the general population, B – lack of synthesis of E5 protein by EV-HPV protects against infections in the general population, C – in epidermodysplasia verruciformis mutations of EVER genes lead to impairment of the ZnT-1/EVER complex, allowing EV HPV infections

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