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Loss-of-function mutations in myosin Vb lead to defects in apical membrane traffic in enterocytes in microvillus inclusion disease. This work shows that decreased numbers of apical CFTR molecules are more active for Cl − secretion resulting in profuse diarrhea because of PKA activation in the presence of physiological glucocorticoid concentrations.

Glucocorticoids and myosin5b loss of function induce heightened PKA signaling in addition to membrane traffic defects