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EVER2 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q8IU68 |
| Other Accession | AAM44454, 25527192 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 81641 Da |
| Application Notes | EVER2 antibody can be used for detection of EVER2 by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 147138 |
|---|---|
| Target/Specificity | TMC8; At least three isoforms of EVER2 are known to exist; this antibody will only recognize the larger isoform. EVER2 has no cross-reactivity to EVER1. |
| Reconstitution & Storage | EVER2 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | EVER2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | TMC8 (HGNC:20474) |
|---|---|
| Function | Acts as a regulatory protein involved in the regulation of numerous cellular processes (PubMed:18158319, PubMed:23429285, PubMed:30068544, PubMed:32917726). Together with its homolog TMC6/EVER1, forms a complex with calcium-binding protein CIB1 in lymphocytes and keratynocytes where TMC6 and TMC8 stabilize CIB1 levels and reciprocally (PubMed:30068544, PubMed:32917726). Together with TMC6, also forms a complex with and activates zinc transporter ZNT1 at the ER membrane of keratynocytes, thereby facilitating zinc uptake into the ER (PubMed:18158319). Also inhibits receptor-mediated calcium release from ER stores and calcium activated and volume regulated chloride channels (PubMed:25220380). Down-regulates the activity of transcription factors induced by zinc and cytokines (PubMed:18158319). Also sequesters TRADD which impairs the recruitment of TRAF2 and RIPK1 in the pro-survival complex I and promotes proapoptotic complex II formation, and may therefore be involved in TNF-induced cell death/survival decisions (PubMed:23429285). |
| Cellular Location | Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Nucleus membrane; Multi-pass membrane protein. Note=Localizes to the ER, Golgi and nucleus membranes in keratinocytes. |
| Tissue Location | Expressed in placenta, prostate and testis. |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
EVER2 Antibody: Epidermodysplasia verruciformis (EV) is an autosomal recessive genodermatosis associated with a high risk of skin cancers resulting from a high susceptibility to infection by specific human papillomaviruses. Mutations in two homologous genes EVER1 and EVER2 cause the majority of EV cases. These two proteins form a complex and interact with the zinc transporter ZnT-1 in the endoplasmic reticulum. Cells lacking EVER2 accumulated higher levels of zinc in the nucleolus and nucleus compare to those cells with and intact EVER2 gene, indicating that one role of EVER2 is to regulate the intracellular distribution of zinc.
References
Ramoz N, Taieb A, Rueda L-A, et al. Evidence for a nonallelic heterogeneity of epidermodysplasia verruciformis with two susceptibility loci mapped to chromosome regions 2p21-p24 and 17q25. J. Invest. Dermatol.2000; 114:1148-53.
Ramoz N, Rueda L-A, Bouadjar B, et al. Mutations in two adjacent novel genes are associated with epidermodysplasia verruciformis. Nat. Genet.2002; 32:579-81.
Lazarczyk M, Pons C, Mendoza J-A, et al. Regulation of cellular zinc balance as a potential mechanism of EVER-mediated protection against pathogenesis by cutaneous oncogenic human papillomaviruses. J. Exp. Med.2008; 205:35-42.
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