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Thus, based on both kinetic data and the use of cardiac glycosides as a tool to identify spike:ACE2 binding, it is possible that a direct spike interaction with ACE2 might be initially responsible for loss of CFTR channel activity
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10.1016/j.cryobiol.2014.03.001 7 Castillo-MartinM.YesteM.PericuestaE.MoratoR.Gutierrez-AdanA.BonetS
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The researchers employed a BALB/c mouse model of AD induced by 1-chloro-2,4-dinitrobenzene (DNCB) and compared the effects of FK506-NIC-CS-NPs to a commercially available ointment (Protopic )
