anti-Transmembrane Channel-Like 8 (TMC8) 抗体

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TMC8 蛋白 (7)和数多这个蛋白质的别的产品。

列出全部抗体 基因 基因ID UniProt
TMC8 147138 Q8IU68
TMC8 688276  
TMC8 217356 Q7TN58
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antibodies-online.cn销售最多的anti-TMC8 抗体

Showing 10 out of 67 products:

产品编号 适用 宿主 标记 应用范围 图像 规格 供应商 交付 价格 详细
非结合性 WB WB Suggested Anti-TMC8 Antibody Titration: 0.2-1 ug/ml ELISA Titer: 1:62500 Positive Control: 721_B cell lysate 100 μL Log in to see 2至3个工作日
$289.00
详细
非结合性 IHC, ELISA Immunohistochemistry analysis of paraffin-embedded human tonsil, using TMC8 Antibody. The picture on the right is treated with the synthesized peptide. 100 μg Log in to see 2至3个工作日
$302.50
详细
非结合性 ELISA, IHC, WB 100 μL Log in to see 16 Days
$181.73
详细
非结合性 WB TMC8 Antibody (N-term) (ABIN658164) western blot analysis in NCI-H292 cell line lysates (35 µg/lane). This demonstrates the TMC8 antibody detected the TMC8 protein (arrow). 400 μL Log in to see 10至11个工作日
$385.00
详细
非结合性 IHC, IHC (p), WB Human Placenta: Formalin-Fixed, Paraffin-Embedded (FFPE) Human Testis: Formalin-Fixed, Paraffin-Embedded (FFPE) 50 μg Log in to see 11至14个工作日
$484.00
详细
非结合性 WB 50 μg Log in to see 11至14个工作日
$551.83
详细
非结合性 ELISA, WB Western blot analysis of TMC8 using HeLa whole cell lysates 100 μL Log in to see 11至12个工作日
$390.77
详细
非结合性 WB 50 μg Log in to see 11至14个工作日
$551.83
详细
非结合性 IHC, ELISA, WB   100 μg Log in to see 15至19个工作日
$527.03
详细
非结合性 ELISA, WB   100 μg Log in to see 15至19个工作日
$527.03
详细

引用最多的anti-TMC8 抗体

  1. Human Polyclonal TMC8 Primary Antibody for IHC (p), WB - ABIN541721 : Ramoz, Rueda, Bouadjar, Montoya, Orth, Favre: Mutations in two adjacent novel genes are associated with epidermodysplasia verruciformis. in Nature genetics 2002 (PubMed)
    Show all 2 Pubmed References

  2. Human Polyclonal TMC8 Primary Antibody for WB - ABIN541734 : Lazarczyk, Pons, Mendoza, Cassonnet, Jacob, Favre: Regulation of cellular zinc balance as a potential mechanism of EVER-mediated protection against pathogenesis by cutaneous oncogenic human papillomaviruses. in The Journal of experimental medicine 2008 (PubMed)
    Show all 2 Pubmed References

  3. Human Polyclonal TMC8 Primary Antibody for IHC, ELISA - ABIN1002274 : 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 (PubMed)
    Show all 3 Pubmed References

更多抗TMC8的相互作用对抗体

Human Transmembrane Channel-Like 8 (TMC8) interaction partners

  1. The relatively high proportion of EV patients without mutation in TMC6/8 indicates the existence of EV-causing mutations in additional, presently unknown gene(s). However, a homozygous TMC8 splice site mutation in our patients resulted in aberrant transcripts which cannot retain the healthy phenotype

  2. The present study did not show any significant association of the EVER1/2 polymorphisms (rs2290907and rs16970849) with cervical cancer.

  3. 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.

  4. 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 tumours that have lost beta-HPV gene expression during progression.

  5. TMC6/EVER1 and TMC8/EVER2 are known to be involved in the development of EV.

  6. A common genetic variation in TMC8 is associated with high-risk HPV infection and head and neck squamous cell carcinoma etiology.

  7. 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.

  8. 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.

  9. TMC8 was found to be localized in the endoplasmic reticulum (ER), where it inhibited receptor mediated Ca(2+) release, activation of Ano1 and volume regulated LRRC8-related Cl(-) currents.

  10. 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.

  11. Loss of the HPV-infection resistance EVER2 protein impairs NF-kappaB signaling pathways in keratinocytes.

  12. 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.

  13. Ever2 interacts with the N-terminal domain of TRADD, impairs the recruitment of TRAF2 and RIPK1 and promotes apoptosis.

  14. EVER2-deficient patients display mild T-cell abnormalities: a significant increase of memory CD4+ and effector memory CD8+ T cells, a bias of the T cell receptor Valphabeta and Vgammadelta repertoires and an increase of skin-homing CD4+ T-cell subsets.

  15. 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

  16. study describes the presence of two previously unreported homozygous mutations in the EVER2 gene in two Italian epidermodysplasia verruciformis patients, each of whom have already developed more than 10 non-melanoma skin cancers

  17. Data support the involvement of the TMC6/8 region in cervix cancer susceptibility.

  18. Results underline the possible relevance of the EVER2/TMC8 single nucleotide polymorphism rs7208422 in influencing susceptibility to beta-papillomaviruses and their oncogenic potential.

  19. Mutations in EVER2 are associated with epidermodysplasia verruciformis.

  20. study reports a novel nonsense mutation of the TMC8 gene in Brazilian patients with epidermodysplasia verruciformis

TMC8 抗原简介

蛋白简介

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.

Gene names and symbols associated with TMC8

  • transmembrane channel like 8 (TMC8) 抗体
  • transmembrane channel-like 8 (Tmc8) 抗体
  • transmembrane channel-like gene family 8 (Tmc8) 抗体
  • EV2 抗体
  • Ever2 抗体
  • EVIN2 抗体
  • mFLJ00400 抗体

Protein level used designations for TMC8

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

GENE ID SPECIES
483342 Canis lupus familiaris
513813 Bos taurus
100031099 Monodelphis domestica
100443950 Pongo abelii
100478575 Ailuropoda melanoleuca
100596943 Nomascus leucogenys
100615612 Pan troglodytes
147138 Homo sapiens
688276 Rattus norvegicus
217356 Mus musculus
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