Fig. 1: ACE2 expression is low in the human lungs and trachea. | Cell Research

Fig. 1: ACE2 expression is low in the human lungs and trachea.

From: AXL is a candidate receptor for SARS-CoV-2 that promotes infection of pulmonary and bronchial epithelial cells

Fig. 1: ACE2 expression is low in the human lungs and trachea.The alternative text for this image may have been generated using AI.

a Schematic of SARS-CoV-2 virion surface S-mediated receptor recognition and membrane fusion. During viral infection, the trimeric S protein is cleaved into S1 and S2 subunits, and the S1 subunits are released during the transition to the post-fusion conformation. The RBD on S1 directly binds to ACE2, while S2 is responsible for membrane fusion. Overview of the human cell landscape at the single-cell level in lung (b) and tracheal cells (e). Abp cell, alveolar bipotent progenitor cell; DC, dendritic cell; EC, endothelial cell; EpC, epithelial cell; MC, macrophages; NK, natural killer cell; SMC, smooth muscle cell. ACE2 expression levels in pulmonary (c, d) and bronchial cells (f, g) were evaluated using the human cell landscape at the single-cell level. Gene expression for each cell type was visualized using tSNE (c, f) and violin plots (d, g). h Eleven lung, liver, kidney, stomach, and neural cell lines were infected with the GFP-labeled SARS-CoV-2 pseudotype. The infection efficiency was evaluated using microscopy images taken at 24 h post infection. The scale bar indicates 250 μm. BF, bright field. The data shown are representative results from three independent experiments (n = 3).

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