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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. Zusätzlich bieten wir Ihnen TMC8 Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal TMC8 Primary Antibody für ELISA, WB - ABIN1002275
Ramoz, Taïeb, Rueda, Montoya, Bouadjar, Favre, Orth: Evidence for a nonallelic heterogeneity of epidermodysplasia verruciformis with two susceptibility loci mapped to chromosome regions 2p21-p24 and 17q25. in The Journal of investigative dermatology 2000
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Human Polyclonal TMC8 Primary Antibody für IHC, ELISA - ABIN1002274
Ramoz, Rueda, Bouadjar, Montoya, Orth, Favre: Mutations in two adjacent novel genes are associated with epidermodysplasia verruciformis. in Nature genetics 2002
Show all 3 Pubmed References
The present study did not show any significant association of the EVER1 (zeige TMC6 Antikörper)/2 polymorphisms (rs2290907and rs16970849) with cervical cancer.
There were no differences in Ever2 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 SNPs in EVER2 may be involved in the development of premalignant skin lesions that harbour beta-HPV, perhaps giving rise to SCC (zeige CYP11A1 Antikörper) tumours that have lost beta-HPV gene expression during progression.
TMC6/EVER1 (zeige TMC6 Antikörper) and TMC8/EVER2 are known to be involved in the development of EV.
A common genetic variation in TMC8 is associated with high-risk HPV infection and head and neck squamous cell carcinoma etiology.
We found a possible correlation between the EVER2 TT genotype and the development of AK, suggesting a potential role of this polymorphism in the development of AK.
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 (zeige TMC6 Antikörper) or EVER2.
TMC8 was found to be localized in the endoplasmic reticulum (ER), where it inhibited receptor mediated Ca(2 (zeige CA2 Antikörper)+) release, activation of Ano1 (zeige ANO1 Antikörper) and volume regulated LRRC8 (zeige LRRC8A Antikörper)-related Cl(-) currents.
Expression of both EVER1 (zeige TMC6 Antikörper) 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 (zeige NFKB1 Antikörper) signaling.
Loss of the HPV-infection resistance EVER2 protein impairs NF-kappaB (zeige NFKB1 Antikörper) signaling pathways in keratinocytes.
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 8 predicted transmembrane domains and 3 leucine zipper motifs.
transmembrane channel-like 8
, FLJ00400 protein-like
, transmembrane channel-like protein 8-like
, epidermodysplasia verruciformis 2
, epidermodysplasia verruciformis protein 2
, transmembrane channel-like protein 8
, uncharacterized protein LOC688276
, epidermodysplasia verruciformis protein 2 homolog