Anti-SARS-CoV-2 ORF10 polyclonal antibody (CABT-CS072)

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
SARS-CoV-2
Immunogen
Synthetic peptide
Conjugate
unconjugated

Target


Alternative Names
SARS-CoV-2 ORF10; SARS-CoV-2; SARS-CoV-2 ORF10 protein

Citations


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References


Molecular Biology of SARS-CoV-2

TURKISH JOURNAL OF IMMUNOLOGY

Authors: Piepoli, Sofia; Shamloo, Bahar; Bircan, Aylin; Adebali, Ogun; Erman, Batu

The Severe Acute Respiratory Syndrome Corona Virus-2 (SARS-CoV-2) has resulted in the COVID-19 pandemic, which is currently wreaking havoc in human societies. To understand how this virus causes disease, the molecular biology of the virus needs to be studied in more detail. There is a large body of work on the molecular strategies of previous coronaviruses that infected humans, which can be directly applied to SARS-CoV-2. In the current review we highlight the novel aspects of the SARS-CoV-2 coronavirus life cycle, and how this and other viruses interact with the biochemistry of the host organism. We provide a discussion of different types of viruses as a background to understand coronaviruses. Specifically, we compare the life cycles of coronaviruses with that of a model retrovirus, the Human Immunodeficiency Virus (HIV). We describe the genomic, transcription and translation control features of coronaviruses with a focus on protein structures and activities that can be selected as molecular targets of therapy.

SARS-CoV-2 Molecular Network Structure

FRONTIERS IN PHYSIOLOGY

Authors: Diaz, Jose

Knowledge about the molecular basis of SARS-CoV-2 infection is incipient. However, recent experimental results about the virus interactome have shown that this single-positive stranded RNA virus produces a set of about 28 specific proteins grouped into 16 non-structural proteins (Nsp1 to Nsp16), four structural proteins (E, M, N, and S), and eight accessory proteins (orf3a, orf6, orf7a, orf7b, orf8, orf9b, orf9c, and orf10). In this brief communication, the network model of the interactome of these viral proteins with the host proteins is analyzed. The statistical analysis of this network shows that it has a modular scale-free topology in which the virus proteins orf8, M, and Nsp7 are the three nodes with the most connections (links). This result suggests the possibility that a simultaneous pharmacological attack on these hubs could assure the destruction of the network and the elimination of the virus.

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