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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. Additionally we are shipping Transmembrane Channel-Like 6 Antibodies (47) and many more products for this protein.
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There were no differences in Ever1 SNPs between head and neck squamous cell carcinoma patients with human papilloma virus (HPV)-positive and HPV-negative tumors, and healthy controls.
Findings suggest that SNP in EVER 1 may be involved in the development of premalignant skin lesions that harbour beta-HPV, perhaps giving rise to SCC (show CYP11A1 Proteins) tumours that have lost beta-HPV gene expression during progression
TMC6/EVER1 and TMC8/EVER2 (show TMC8 Proteins) are known to be involved in the development of EV.
TMC6 variants are associated with diminished age-of-onset of P. aeruginosa airway infection in children with cystic fibrosis (show S100A8 Proteins).
EV is also a rare autosomal recessive genodermatosis involving susceptibility to human papillomavirus (HPV) infections and squamous cell carcinoma, caused in most cases by homozygous mutations in EVER1 or EVER2 (show TMC8 Proteins).
Expression of both EVER1 and EVER2 (show TMC8 Proteins) in B cells is activated immediately after Epstein-Barr virus (EBV) infection, whereas at later stages, it is strongly repressed by latent membrane protein 1-activated NF-kappaB (show NFKB1 Proteins) signaling.
Data support the involvement of the TMC6/8 region in cervix cancer susceptibility.
Mutations in EVER1 are associated with epidermodysplasia verruciformis.
four mutations in recurrent respiratory papillomatosis patients might indicate that EVER 1 alleles are not associated with susceptibility to RRP (show RRBP1 Proteins)
The growing number of mutations in epidermodysplasia verruciformis (EV) pedigrees supports the hypothesis that EVER1 and EVER2 (show TMC8 Proteins) are the molecular basis of EV.
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 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. This gene encodes a transmembrane channel-like protein with 10 transmembrane domains and 2 leucine zipper motifs.
transmembrane channel-like 6
, epidermodysplasia verruciformis 1
, transmembrane channel-like protein 6
, transmembrane channel-like protein 6-like
, epidermodysplasia verruciformis protein 1
, expressed in activated T/LAK lymphocytes
, protein LAK-4