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。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
MAVS Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | Q7Z434 |
| Other Accession | NP_065797.2 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 56528 Da |
| Antigen Region | 477-505 aa |
| Gene ID | 57506 |
|---|---|
| Other Names | Mitochondrial antiviral-signaling protein, MAVS, CARD adapter inducing interferon beta, Cardif, Interferon beta promoter stimulator protein 1, IPS-1, Putative NF-kappa-B-activating protein 031N, Virus-induced-signaling adapter, VISA, MAVS, IPS1, KIAA1271, VISA |
| Target/Specificity | This MAVS antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 477-505 amino acids from the C-terminal region of human MAVS. |
| Dilution | WB~~1:2000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. 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 | MAVS Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | MAVS {ECO:0000303|PubMed:16125763, ECO:0000312|HGNC:HGNC:29233} |
|---|---|
| Function | Adapter required for innate immune defense against viruses (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20127681, PubMed:20451243, PubMed:21170385, PubMed:23087404, PubMed:27992402, PubMed:33139700, PubMed:37582970). Acts downstream of DHX33, RIGI and IFIH1/MDA5, which detect intracellular dsRNA produced during viral replication, to coordinate pathways leading to the activation of NF-kappa-B, IRF3 and IRF7, and to the subsequent induction of antiviral cytokines such as IFNB and RANTES (CCL5) (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20127681, PubMed:20451243, PubMed:20628368, PubMed:21170385, PubMed:23087404, PubMed:25636800, PubMed:27736772, PubMed:33110251). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state (PubMed:20451243). Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response (PubMed:20451243). May activate the same pathways following detection of extracellular dsRNA by TLR3 (PubMed:16153868). May protect cells from apoptosis (PubMed:16125763). Involved in NLRP3 inflammasome activation by mediating NLRP3 recruitment to mitochondria (PubMed:23582325). |
| Cellular Location | Mitochondrion outer membrane; Single-pass membrane protein. Mitochondrion. Peroxisome |
| Tissue Location | Present in T-cells, monocytes, epithelial cells and hepatocytes (at protein level). Ubiquitously expressed, with highest levels in heart, skeletal muscle, liver, placenta and peripheral blood leukocytes. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Double-stranded RNA viruses are recognized in a cell type-dependent manner by the transmembrane receptor TLR3 (MIM 603029) or by the cytoplasmic RNA helicases MDA5 (MIM 606951) and RIGI (ROBO3; MIM 608630). These interactions initiate signaling pathways that differ in their initial steps but converge in the activation of the protein kinases IKKA (CHUK; MIM 600664) and IKKB (IKBKB; MIM 603258), which activate NFKB (see MIM 164011), or TBK1 (MIM 604834) and IKKE (IKBKE; MIM 605048), which activate IRF3 (MIM 603734). Activated IRF3 and NFKB induce transcription of IFNB (IFNB1; MIM 147640). For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein TRIF (TICAM1; MIM 607601). For RIGI, the intermediary protein is mitochondria-bound IPS1 (Sen and Sarkar, 2005 [PubMed 16239922]).
REFERENCES
Sebastiani, P., et al. Science (2010) In press :
Wang, X., et al. Cell. Mol. Immunol. 7(5):341-348(2010)
Graef, K.M., et al. J. Virol. 84(17):8433-8445(2010)
Wei, C., et al. J. Immunol. 185(2):1158-1168(2010)
Onoguchi, K., et al. PLoS Pathog. 6 (7), E1001012 (2010) :
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