SARS-CoV-2-Structural Genes

structure proteins covid-19

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SARS-CoV-2-Cellular Receptor Genes

Spike full-length or fragments - Matrix - Envelope - Nucleocapsid

SARS-CoV-2 (or 2019-nCoV) is the causative agent for COVID-19. This virus belongs to lineage B of the β-coronavirus genus [1]. Coronaviruses are relatively large enveloped, positive-sense, single-stranded RNA (~30 kb) viruses. The SARS-CoV-2 genome encodes four structural proteins and other accessory or non-structural proteins (including the viral pp1a-pp1ab replicase, the 3C-like protease (3CLpro), the papain-like protease (PLpro), and the RNA-dependent RNA-polymerase RdRp)) [2, 3].

SARS-CoV-2 structural proteins are:

  • Spike (S) forms large trimeric structures that are essential for entry into host cells upon receptor binding and membrane fusion. Spike proteins are targeted by host neutralizing antibodies.
  • Envelope (E) is only present in small quantities and most likely forms ion channels. E proteins are not necessarily needed for viral replication but are essential for infectivity and pathogenesis.
  • Matrix/Membrane (M) is the most abundant structural protein of the virus. M proteins are responsible for membrane curvature of the viral envelope, notably through their interaction with the E proteins.
  • Nucleocapsid (N) binds to the viral RNA genome and ensures the maintenance of the RNA in a ‘beads-on-a-string’ conformation.


Depending on your applications, InvivoGen offers SARS-CoV-2-Structural Genes cloned into mammalian expression plasmids, or into production plasmids with a His- or Fc-tag.




1. Zhu, N. et al., 2020. A Novel Coronavirus from Patients with Pneumonia in China, 2019. N Engl J Med 382, 727-733.
2. Fehr, A.R. & Perlman, S. 2015. Coronaviruses: an overview of their replication and pathogenesis. Methods Mol Biol 1282, 1-23.
3. Zhou, P. et al., 2020. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270-273.

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