Cell culture adaptation of SARS-CoV-2 is prevented on human airway cells with an active serine protease-mediated entry pathway, allowing the production of genetically stable virus stocks for laboratory experiments.
Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.
Cell replenishment within the airways is governed by the random division of a population of basal progenitor cells, in a process that is accelerated in smokers.
Notch ligands from the Delta and Jagged families have distinct roles in epithelial progenitor cell fate of extrapulmonary and intrapulmonary airways and differentially restrict expansion of the neuroendocrine microenvironment.
Formation and cell pole-localization of chemotactic signaling-arrays is a coupled process mediated by ParP, which drives localized array-assembly and regulates the localization-dynamics of its network constituents.
Whereas SARS-CoV-2 utilizes cathepsins to enter most cell lines, human airway organoids revealed that entry into relevant cells is dependent on serine proteases, which can be targeted for treatment.
The chloride channel Ano1/Tmem16a plays an essential and non-redundant role in the developing airway by inhibiting mucus cell hyperplasia and promoting proper immune function of the airway mucosal barrier.
Mycobacterium tuberculosis penetrates the airway mucosa through M cells via the mycobacterial virulence factor EsxA and the host M cell surface receptor scavenger receptor B1.
Cas12a CRISPR arrays are sensitive to the GC content of their spacers, but AT-rich separator sequences successfully remove this disruptive effect and enable enhanced multiplexed gene targeting and activation.
