Objective To investigate whether the partially C-terminal deletion of NR2A subunit alters the surface expression and channel function of NMDA receptors in both HEK293 cells and cultured hippocampal neurons of rats. Methods Four plasmids for NR2A mutants with N-terminally GFP-tagged and C-terminal deletion NR2A?C1(?897L-1017S),NR2A?C2(?1024D-1142P),NR2A?C3(?1149D-1347G),and NR2A?C4(?1354S-1464V) were generated,and transfected into HEK293 cells and hippocampal neurons in culture.Surface staining was performed using anti-GFP antibody and Cy3 conjugated secondary antibody.Glutamate evoked currents were also detected using whole-cell recording. Results Positive surface staining was found for all the HEK293 cell co-transfected NR1-1a/NR2A?C1,NR1-1a/NR2A?C2,NR1-1a/NR2A?C3 or NR1-1a/NR2A?C4,and quantitative analysis showed no significant decrease in surface expression level when compared to that from NR1-1a/NR2A transfection.Glutamate-evoked currents were recorded in HEK293 cells co-transfected with NR1-1a/NR2A?C2 or NR1-1a/NR2A?C4.Surface expression level of NMDA receptor clusters on dendrites was significantly decreased in the neurons transfected with NR2A?C1,NR2A?C2 or NR2A?C3 than in those transfected with NR2A.Conclusion C-terminal deletion of NR2A subunit differentially effects surface expression of NMDA receptors in HEK293 cells and in hippocampal neurons in culture.

The three known highly pathogenic human coronaviruses are severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Human highly pathogenic coronaviruses are composed of non-structural proteins, structural proteins, accessory proteins and ribonucleic acid. Viral particles recognize host receptors via spike glycoprotein (S protein), enter host cells by membrane fusion, replicate in host cells through large replication-transcription complexes, and promote proliferation by interfering with and suppressing the host's immune response. Highly pathogenic human coronaviruses are hosted by humans and vertebrates. Viral particles are transmitted through droplets, contact and aerosols or likely through digestive tract, urine, eyes and other routes. This review discusses the mechanisms of replication and transmission of highly pathogenic human coronaviruses providing basis for future studies on interrupting the transmission and pathogenicity of these pathogenic viruses.
Animals ; Betacoronavirus ; Coronavirus Infections ; Humans ; Middle East Respiratory Syndrome Coronavirus ; Pandemics ; Pneumonia, Viral ; Spike Glycoprotein, Coronavirus

The three known human highly pathogenic coronaviruses are severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus, (MERS-CoV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Human highly pathogenic coronaviruses are composed of non-structural proteins, structural proteins and accessory proteins. Viral particles recognize host receptors via spike glycoprotein (S protein), enter host cells by membrane fusion, replicate in host cells through large replication-transcription complexes, and promote proliferation by interfering with and suppressing the host's immune response. Human highly pathogenic coronaviruses are hosted by humans and vertebrates. Viral particles are transmitted through droplets, contact and aerosols or likely through digestive tract, urine, eyes and other routes. This review discusses the mechanisms of proliferation and transmission of highly pathogenic human coronaviruses based on the results of existing research, providing basis for future study on interrupting the transmission and pathogenicity of human highly pathogenic coronaviruses.
Animals ; Betacoronavirus ; physiology ; Coronavirus Infections ; immunology ; transmission ; virology ; Humans ; Middle East Respiratory Syndrome Coronavirus ; physiology ; Pandemics ; Pneumonia, Viral ; immunology ; transmission ; virology ; SARS Virus ; physiology ; Virus Replication ; physiology