RSAD2 Rabbit Polyclonal Antibody
Konjugasyon: Unconjugated
Rabbit polyclonal Antibody
Uygulama
Reaktivite
Human,Rat,Mouse
Gen Adı
RSAD2
Saklama
Aliquot and store at -20°C (valid for 12 months). Avoid freeze/thaw cycles.
Özet
| Ürün Adı | RSAD2 Rabbit Polyclonal Antibody |
| Açıklama | Rabbit polyclonal Antibody |
| Konak | Rabbit |
| Reaktivite | Human,Rat,Mouse |
| Konjugasyon | Unconjugated |
| Modifikasyon | Unmodified |
| İzotip | IgG |
| Klonalite | Polyclonal |
| Form | Liquid |
| Konsantrasyon | Unconjugated |
| Saklama | Aliquot and store at -20°C (valid for 12 months). Avoid freeze/thaw cycles. |
| Nakliye | Ice bags. |
| Tampon | Liquid in PBS containing 50% glycerol, 0.5% protective protein and 0.02% New type preservative N. |
| Saflaştırma | Affinity purification |
Antijen Bilgisi
| Gen Adı | RSAD2 |
| Alternatif İsimler | RSAD2; CIG5; Radical S-adenosyl methionine domain-containing protein 2; Cytomegalovirus-induced gene 5 protein; Viperin; Virus inhibitory protein, endoplasmic reticulum-associated, interferon-inducible |
| Gen Kimliği | 91543 |
| SwissProt Kimliği | Q8WXG1 |
| İmmünojen | The antiserum was produced against synthesized peptide derived from the N-terminal region of human RSAD2. AA range:21-70 |
Uygulama
| Uygulama | WB,IHC,ICC/IF,ELISA |
| Seyreltme Oranı | WB 1:500-1:2000,IHC 1:100-1:300,ICC/IF 1:50-1:200,ELISA 1:10000-1:20000 |
| Moleküler Ağırlık | 42kDa |
Araştırma Alanı
| Microbiology; Interspecies Interaction; Host Virus Interaction; Immunology; Immune System Diseases; Antiviral Signaling |
Arka Plan
| cofactor:Binds 1 4Fe-4S cluster. The cluster is coordinated with 3 cysteines and an exchangeable S-adenosyl-L-methionine.,function:Involved in antiviral defense. May impair virus budding by disrupting lipid rafts at the plasma membrane, a feature which is essential for the budding process of many viruses. Acts through binding with and inactivating FPPS, an enzyme involved in synthesis of cholesterol, farnesylated and geranylated proteins, ubiquinones dolichol and heme. Plays a major role in the cell antiviral state induced by type I and type II interferon. Displays antiviral effect against HIV-1 virus, hepatitis C virus, human cytomegalovirus, and aphaviruses, but not vesiculovirus.,induction:By interferon type I, type II and LPS. Little or no induction by interferon gamma is observed in monocytic cell lines. Induced by infection with human cytomegalovirus (HMCV), hepatitis C virus, yellow fever virus and Sendai virus, presumably through type I interferon pathway.,miscellaneous:Up-regulated in atherosclerosis. Latent viruses like HCMV may be involved in atherogenesis by initiating local inflammation. This may induce up-regulation of antiviral gene RSAD2, which modulates lipids synthesis, and thus could play a role in abnormal lipid accumulation leading to atherosclerosis.,similarity:Belongs to the RSAD2 family.,subcellular location:Probably associates with the cytosolic side of the endoplasmic reticulum. Infection with human cytomegalovirus (HCMV) causes relocation to the Golgi apparatus and to cytoplasmic vacuoles which also contain HCMV proteins glycoprotein B and pp28.,subunit:Interacts with FPPS.,cofactor:Binds 1 4Fe-4S cluster. The cluster is coordinated with 3 cysteines and an exchangeable S-adenosyl-L-methionine.,function:Involved in antiviral defense. May impair virus budding by disrupting lipid rafts at the plasma membrane, a feature which is essential for the budding process of many viruses. Acts through binding with and inactivating FPPS, an enzyme involved in synthesis of cholesterol, farnesylated and geranylated proteins, ubiquinones dolichol and heme. Plays a major role in the cell antiviral state induced by type I and type II interferon. Displays antiviral effect against HIV-1 virus, hepatitis C virus, human cytomegalovirus, and aphaviruses, but not vesiculovirus.,induction:By interferon type I, type II and LPS. Little or no induction by interferon gamma is observed in monocytic cell lines. Induced by infection with human cytomegalovirus (HMCV), hepatitis C virus, yellow fever virus and Sendai virus, presumably through type I interferon pathway.,miscellaneous:Up-regulated in atherosclerosis. Latent viruses like HCMV may be involved in atherogenesis by initiating local inflammation. This may induce up-regulation of antiviral gene RSAD2, which modulates lipids synthesis, and thus could play a role in abnormal lipid accumulation leading to atherosclerosis.,similarity:Belongs to the RSAD2 family.,subcellular location:Probably associates with the cytosolic side of the endoplasmic reticulum. Infection with human cytomegalovirus (HCMV) causes relocation to the Golgi apparatus and to cytoplasmic vacuoles which also contain HCMV proteins glycoprotein B and pp28.,subunit:Interacts with FPPS., |
