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SARS Coronavirus Nucleoprotein (N-Term, Mid)

$447.95$1,680.20 excl. VAT

SARS Coronavirus Nucleoprotein (N-Term, Mid) is a recombinant protein (also known as the nucleocapsid core antigen) comprising the N-term fused to an immunodominant region from the middle of the protein (aa 1-49, 192-220). It is manufactured in E. coli, with greater than 95% purity.

SARS CORONAVIRUS NUCLEOPROTEIN (N-TERM, MID)

SARS Coronavirus Nucleoprotein (N-Term, Mid) is a recombinant protein (also known as the nucleocapsid core antigen) comprising the N-term fused to an immunodominant region from the middle of the protein. It is manufactured in E. coli with greater than 95% purity.

 

PRODUCT DETAILS

  • SARS Coronavirus Nucleoprotein (N-Term, Mid).
  • Recombinant protein manufactured in E. coli.
  • Contains Nucleocapsid core protein, 1-49, 192-220 amino acids immunodominant regions. The 2 regions are separated with 3 glycine residues.
  • Purity >95% as determined by 10% PAGE (Coomassie staining).
  • For use in ELISA and other immunoassays.

 

BACKGROUND

Coronaviruses (CoV) cause acute and chronic respiratory, enteric, and central nervous system (CNS) diseases in many species of animals, including humans (McIntosh, 1974). Prior to the emergence of SARS-CoV, there were two prototype human coronaviruses, OC43 and 229E, both etiologic agents of the common cold (Weiss and Navas-Martin, 2005). However, severe acute respiratory syndrome (SARS) was the first example of serious illness in humans caused by a coronavirus (Rota et al., 2003). An outbreak of SARS-CoV began in the Guangdong Province of China, and spread rapidly to more than 30 countries during 2003. SARS has an acute onset, is highly transmissible and has a high case-mortality rate (approximately 10%) (Peiris et al., 2003; Ksiazek et al., 2003). DSARS infection results in respiratory tract pathological changes and an over-exuberant host immune response. This mediates immunopathological damage of the lungs and other organs, and pulmonary fibrosis. Mortality is caused primarily by extensive lung damage and severe lymphopenia (Tsui et al., 2003). Approximately 10% of individuals (6.8% of patients younger and 55% of patients older than 60 years of age) with clinical symptoms died as a consequence of immunopathological lung damage, caused by a hyperactive antiviral immune response (Nicholl et al., 2003).

SARS-CoV nucleocapsid protein (SARS-CoV NP) is an extensively phosphorylated, highly basic, vital structural protein with the primary function of forming a helical ribonucleoprotein complex with viral RNA (vRNA). This complex comprises the core structure of the SARS-CoV virion. A number of different functions have been ascribed to SARS-CoV NP, including packaging, transcription, and replication. SARS-CoV NP shows intrinsic multimerization and interacts with M protein, suggesting that NP is both critical to formation of the viral nucleocapsid core and is involved in virion assembly (Wang et al., 2010).

 

REFERENCES

  • Ksiazek et al. (2003). A Novel Coronavirus Associated with Severe Acute Respiratory Syndrome. N Engl J Med, 348: 1953-1966.
  • McIntosh, K. (1974). Coronaviruses: a comparative review. Curr. Top. Microbiol. Immunol. 63:85-129.
  • Nicholl et al. (2003). Lung pathology of fatal severe acute respiratory syndrome. Lancet, 361: 1773-1778.
  • Peiris et al. (2003). Coronavirus as a possible cause of severe acute respiratory syndrome. The Lancet, 361: 1319-1326.
  • Rota et al. (2003). Characterization of a novel coronavirus associated with severe acute respiratory syndrome. Science 300:1394-1399.
  • Tsui et al. (2003). Severe acute respiratory syndrome: clinical outcome and prognostic correlates. Emerg Infect Dis, 9: 1064-1069.
  • Wang et al. (2010). Interactions of SARS Coronavirus Nucleocapsid Protein with the host cell proteasome subunit p42. Virology Journal volume 7, Article number: 99.
  • Weiss and Navas-Martin (2005). Coronavirus Pathogenesis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus. Microbiol Mol Biol Rev. 69(4): 635–664.

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