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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. 再加上，我们可以发Transmembrane Channel-Like 6 蛋白 (5)和数多这个蛋白质的别的产品。
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Human Polyclonal TMC6 Primary Antibody for IHC (p), WB - ABIN541706
Majewski, Jab?o?ska, Orth: Epidermodysplasia verruciformis. Immunological and nonimmunological surveillance mechanisms: role in tumor progression. in Clinics in dermatology 1997
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Human Polyclonal TMC6 Primary Antibody for IHC (p), WB - ABIN541708
Keresztes, Mutai, Heller: TMC and EVER genes belong to a larger novel family, the TMC gene family encoding transmembrane proteins. in BMC genomics 2003
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The present study did not show any significant association of the EVER1/2 polymorphisms (rs2290907and rs16970849) with cervical cancer.
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 tumours that have lost beta-HPV gene expression during progression
TMC6/EVER1 and TMC8/EVER2 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.
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.
Expression of both EVER1 and EVER2 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 signaling.
We report a case of Merkel cell polyomavirus detection in the skin of a patient with epidermodysplasia verruciformis (EDV) and a family history remarkable for an unusual inheritance pattern for EDV.
EVER proteins appear as key components of the activation-dependent regulation of Zn(2+) concentration in T cells. However, the impact of EVER-deficiency in T cells on EV pathogenesis remains to be elucidated
Data support the involvement of the TMC6/8 region in cervix cancer susceptibility.
Mutations in EVER1 are associated with epidermodysplasia verruciformis.
Nonsense mutations of EVER1gene is associated with epidermodysplasia verruciformis
four mutations in recurrent respiratory papillomatosis patients might indicate that EVER 1 alleles are not associated with susceptibility to RRP
The growing number of mutations in epidermodysplasia verruciformis (EV) pedigrees supports the hypothesis that EVER1 and EVER2 are the molecular basis of EV.
HPV16 E5 protein binds to EVER and ZnT-1 and blocks their negative regulation
epidermodysplasia verruciformis in a father and a son with typical histologic and clinical findings that occur in the absence of mutations in EVER1
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