SARS Envelope Protein (a.a. 1-76) [GST] (DAG2411)

Recombinant SARS Envelope Protein (a.a. 1-76) from E. coli [GST]

Product Overview
The E.coli derived 43 kDa recombinant protein contains the N-terminus Envelope protein 1-76 amino acids immunodominant regions.
Nature
Recombinant
Tag/Conjugate
Unconjugated
Alternative Names
SARS Envelope Protein; SARS; SARS E Protein; SARS E
Procedure
None
Purity
> 95%, based on SDS PAGE
Format
Liquid
Buffer
50mM Tris-HCl, 60mM NaCl and 50% glycerol
Preservative
None
Storage
2-8°C short term, -20°C long term
Introduction
A novel coronavirus has been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive stranded RNA approximately 27 to 31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2.
Keywords
SARS Envelope Protein; SARS; SARS E Protein; SARS E

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References


The M, E, and N Structural Proteins of the Severe Acute Respiratory Syndrome Coronavirus Are Required for Efficient Assembly, Trafficking, and Release of Virus-Like Particles

JOURNAL OF VIROLOGY

Authors: Siu, Y. L.; Teoh, K. T.; Lo, J.; Chan, C. M.; Kien, F.; Escriou, N.; Tsao, S. W.; Nicholls, J. M.; Altmeyer, R.; Peiris, J. S. M.; Bruzzone, R.; Nal, B.

The production of virus-like particles (VLPs) constitutes a relevant and safe model to study molecular determinants of virion egress. The minimal requirement for the assembly of VLPs for the coronavirus responsible for severe acute respiratory syndrome in humans (SARS-CoV) is still controversial. Recent studies have shown that SARS-CoV VLP formation depends on either M and E proteins or M and N proteins. Here we show that both E and N proteins must be coexpressed with M protein for the efficient production and release of VLPs by transfected Vero E6 cells. This suggests that the mechanism of SARS-CoV assembly differs from that of other studied coronaviruses, which only require M and E proteins for VLP formation. When coexpressed, the native envelope trimeric S glycoprotein is incorporated onto VLPs. Interestingly, when a fluorescent protein tag is added to the C-terminal end of N or S protein, but not M protein, the chimeric viral proteins can be assembled within VLPs and allow visualization of VLP production and trafficking in living cells by state-of-the-art imaging technologies. Fluorescent VLPs will be used further to investigate the role of cellular machineries during SARS-CoV egress.

Pathophysiology of multi-organ damage in SARS-CoV-2 infection

ACTA PEDIATRICA DE MEXICO

Authors: Tiburcio Lopez-Perez, Gerardo; Patricia Ramirez-Sandoval, Maria de Lourdes; Solyenetzin Torres-Altamirano, Mayra

SARS-CoV-2 could originate from unknown bats or intermediate hosts and cross the species barrier to humans. Virus-host interactions affect viral entry and replication. The virus genome encodes four essential structural proteins, the spike glycoprotein, the small envelope protein, the matrix proteins, and the nucleocapsid protein. The SARS-CoV-2 glycoprotein S binds to the host cell receptors of the enzyme, the conversion of angiotensin 2 (ACE2), which is a critical step for virus entry. It is expressed more in men than in women, probably by estradiol and testosterone that can influence ACE activity in different ways. In the viremia phase, it passes from the salivary glands and mucous membranes, especially the nasal and larynx, to the lungs and other organs with the same ACE2 receptors, such as the heart, liver, and even the central nervous system. It can reach the intestines, which can explain the symptoms and is detected in the stool from the beginning of the infection. Comorbidities such as immunodeficient status, old age, systemic arterial hypertension, diabetes mellitus or chronic lung diseases, obesity or smoking are key to viral pathogenesis. When the immune system is inefficient to effectively control the virus in the acute phase, it can evolve into a macrophage activation syndrome that results in the dreaded cytokine storm that puts the patient in a very critical condition. Understanding the pathophysiology of SARS-CoV-2 infection is the cornerstone to provide timely diagnosis and implement appropriate treatment for patients, limiting the spread of the virus and ultimately eliminating the presence of the virus in humanity.

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