SARS-CoV-2 (2019-nCoV) Spike S1 Subunit, Recombinant, aa16-685, His-Tag

An epidemic of acute respiratory syndrome in humans, which appeared in Wuhan, China in December 2019, was caused by a novel coronavirus (SARS-CoV-2). This disease was named as "Coronavirus Disease 2019" (COVID19). This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERSCoV. The genome of this and other emerging pathogenic human CoVs encodes four major structural proteins [spike (S), envelope (E), membrane (M), and nucleocapsid (N)], approximately 16 nonstructural proteins (nsp1–16), and five to eight accessory proteins. Among them, the S protein plays an essential role in viral attachment, fusion, entry, and transmission. It comprises an N-terminal S1 subunit responsible for virus–receptor binding and a C-terminal S2 subunit responsible for virus–cell membrane fusion. S1 is further divided into an N-terminal domain (NTD) and a receptor-binding domain (RBD). SARS-CoV-2 and SARS-CoV bind angiotensinconverting enzyme 2 (ACE2) while MERS-CoV binds dipeptidyl peptidase 4 (DPP4), as receptors on the host cell|expressing ACE2 (e.g., pneumocytes, enterocytes) or DPP4 (e.g., liver or lung cells including Huh-7, MRC-5, and Calu-3). During infection, CoV first binds the host cell through interaction between its S1-RBD and the cell|membrane receptor, triggering conformational changes in the S2 subunit that result in virus fusion and entry into the target cell. ||Recombinant protein corresponding to aa16-685 from SARS-CoV-2 (2019-nCoV) Spike S1 Subunit, fused to His-Tag at C-terminal, expressed in HEK293 cells.||Molecular Weight: |~76.2kD||Biological Activity:|Measured by its binding ability in a functional ELISA with Human ACE-2. ||Amino Acid Sequence:|<DGSM>VNLTTR TQLPPAYTNS FTRGVYYPDK VFRSSVLHST QDLFLPFFSN VTWFHAIHVS GTNGTKRFDN PVLPFNDGVY FASTEKSNII RGWIFGTTLD SKTQSLLIVN NATNVVIKVC EFQFCNDPFL GVYYHKNNKS WMESEFRVYS SANNCTFEYV SQPFLMDLEG KQGNFKNLRE FVFKNIDGYF KIYSKHTPIN LVRDLPQGFS ALEPLVDLPI GINITRFQTL LALHRSYLTP GDSSSGWTAG AAAYYVGYLQ PRTFLLKYNE NGTITDAVDC ALDPLSETKC TLKSFTVEKG IYQTSNFRVQ PTESIVRFPN ITNLCPFGEV FNATRFASVY AWNRKRISNC VADYSVLYNS ASFSTFKCYG VSPTKLNDLC FTNVYADSFV IRGDEVRQIA|PGQTGKIADY NYKLPDDFTG CVIAWNSNNL DSKVGGNYNY LYRLFRKSNL KPFERDISTE IYQAGSTPCN GVEGFNCYFP LQSYGFQPTN GVGYQPYRVV VLSFELLHAP ATVCGPKKST NLVKNKCVNF NFNGLTGTGV LTESNKKFLP FQQFGRDIAD TTDAVRDPQT LEILDITPCS FGGVSVITPG TNTSNQVAVL YQDVNCTEVP VAIHADQLTP TWRVYSTGSN VFQTRAGCLI GAEHVNNSYE CDIPIGAGIC ASYQTQTNSP RRAR<HHHHHH>||Storage and Stability: |May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 6 months after receipt at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.