H9784
Hepatitis C virus NS4 antigen−Rhodamine
~1 mg/mL, ≥95% (SDS-PAGE), recombinant, expressed in E. coli, solution
recombinant
expressed in E. coli
Quality Level
Assay
≥95% (SDS-PAGE)
form
solution
mol wt
19 kDa (plus 114 kDa β-Gal tag)
concentration
~1 mg/mL
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
Gene Information
hepatitis C virus ... HCVgp1(951475)
General description
β-gal fused at N-terminus
HCVgp1 (hepatitis C virus glycoprotein 1), also referred to as polyprotein, is crucial for the induction of double-membrane vesicles, which are sites of HCV RNA amplification. The amino terminal of polyprotein contains the structural proteins core, envelope protein 1 (E1) and E2. The proteolytic cleavage of polyprotein results in the formation of 10 mature viral proteins, including NS4 (non-structural 4).
Biochem/physiol Actions
NS4 (non-structural 4) mainly acts a cofactor for the NS3 serine protease, which is needed for the cleavage of the non-structural area of the polyprotein. It also suppresses host cell translation as well as proliferation. In addition, it induces anti-inflammatory cytokines and thereby suppresses cellular immune responses.
Positive control for HCV antibodies.
Physical form
Solution in 8 M urea, 20 mM tris-HCl, pH 8.0, and 10 mM 2-mercaptoethanol.
Other Notes
HCV NS4a+b [1658-1863]-Galactosidase-tagged, rhodamine conjugate.
Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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R Bartenschlager et al.
Journal of virology, 69(12), 7519-7528 (1995-12-01)
Processing of the hepatitis C virus polyprotein is mediated by host cell signalases and at least two virally encoded proteinases. Of these, the serine-type proteinase encompassing the amino-terminal one-third of NS3 is responsible for cleavage at the four sites carboxy
Miriam T Brady et al.
European journal of immunology, 33(12), 3448-3457 (2003-11-25)
The majority of hepatitis C virus (HCV) infections become chronic, despite the presence of HCV-specific cellular and humoral immune responses. We have previously suggested that IL-10-secreting antigen-specific regulatory T cells may contribute to viral persistence, and demonstrate here that peripheral
Inés Romero-Brey et al.
mBio, 6(4), e00759-e00759 (2015-07-15)
Induction of membrane rearrangements in the cytoplasm of infected cells is a hallmark of positive-strand RNA viruses. These altered membranes serve as scaffolds for the assembly of viral replication factories (RFs). We have recently shown that hepatitis C virus (HCV)
Margaret A Scull et al.
PLoS pathogens, 11(11), e1005297-e1005297 (2015-11-21)
The hepatitis C virus (HCV) p7 protein is required for infectious virus production via its role in assembly and ion channel activity. Although NMR structures of p7 have been reported, the location of secondary structural elements and orientation of the
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