癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
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Fagilis (IFITM3) Antibody (Center)
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 文献引用 : 1
- 实验流程
- 背景知识
Application 
| WB, E |
|---|---|
| Primary Accession | Q01628 |
| Other Accession | Q9CQW9, Q99J93, Q01629, P13164 |
| Reactivity | Human |
| Predicted | Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 14632 Da |
| Antigen Region | 64-93 aa |
| Gene ID | 10410 |
|---|---|
| Other Names | Interferon-induced transmembrane protein 3, Dispanin subfamily A member 2b, DSPA2b, Interferon-inducible protein 1-8U, IFITM3 |
| Target/Specificity | This Fagilis (IFITM3) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 64-93 amino acids from the Central region of human Fagilis (IFITM3). |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Fagilis (IFITM3) Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | IFITM3 (HGNC:5414) |
|---|---|
| Function | IFN-induced antiviral protein which disrupts intracellular cholesterol homeostasis. Inhibits the entry of viruses to the host cell cytoplasm by preventing viral fusion with cholesterol depleted endosomes. May inactivate new enveloped viruses which buds out of the infected cell, by letting them go out with a cholesterol depleted membrane. Active against multiple viruses, including influenza A virus, SARS coronaviruses (SARS-CoV and SARS-CoV-2), Marburg virus (MARV), Ebola virus (EBOV), Dengue virus (DNV), West Nile virus (WNV), human immunodeficiency virus type 1 (HIV-1), hepatitis C virus (HCV) and vesicular stomatitis virus (VSV) (PubMed:26354436, PubMed:33239446, PubMed:33270927). Can inhibit: influenza virus hemagglutinin protein- mediated viral entry, MARV and EBOV GP1,2-mediated viral entry, SARS- CoV and SARS-CoV-2 S protein-mediated viral entry and VSV G protein- mediated viral entry (PubMed:33270927). Plays a critical role in the structural stability and function of vacuolar ATPase (v-ATPase). Establishes physical contact with the v-ATPase of endosomes which is critical for proper clathrin localization and is also required for the function of the v-ATPase to lower the pH in phagocytic endosomes thus establishing an antiviral state. In hepatocytes, IFITM proteins act in a coordinated manner to restrict HCV infection by targeting the endocytosed HCV virion for lysosomal degradation (PubMed:26354436). IFITM2 and IFITM3 display anti-HCV activity that may complement the anti-HCV activity of IFITM1 by inhibiting the late stages of HCV entry, possibly in a coordinated manner by trapping the virion in the endosomal pathway and targeting it for degradation at the lysosome (PubMed:26354436). Exerts opposing activities on SARS-CoV-2, including amphipathicity-dependent restriction of virus at endosomes and amphipathicity-independent enhancement of infection at the plasma membrane (PubMed:33270927). |
| Cellular Location | Cell membrane; Single-pass type II membrane protein. Late endosome membrane; Single-pass type II membrane protein. Early endosome membrane; Single-pass type II membrane protein Lysosome membrane; Single-pass type II membrane protein. Cytoplasm, perinuclear region. Note=Co-localizes with BRI3 isoform 1 at the perinuclear region. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The family of interferon-induced transmembrane protein (Ifitm/mil/fragilis) cell surface proteins may modulate cell adhesion and influence cell differentiation.
REFERENCES
Tanaka,S.S., Dev. Cell 9 (6), 745-756 (2005)
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