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You are studying a transporter found only in the apical plasma membrane of epithelial cells. You treat the epithelial cells with a synthetic peptide that is similar to the extracellular domain of a tight junction protein. The transporter is now found in both the apical and basolateral domains of the plasma membrane. What is the most likely mechanism by which the peptide disturbs the localization of the transporter?

How do you predict an inhibitor of H+ pumps would affect the delivery and release of cholesterol within cells via endocytosis?

Which statement about protein kinase A (PKA) is false?

Which hormone is involved in Ca2+ metabolism and bone growth?

As discussed in this section, mutations in the LDL receptor can cause familial hypercholesterolemia. However, mutations in apolipoprotein B100 have also been discovered that cause hypercholesterolemia. For example, mutation of arginine-3500 to glutamine (R3500Q) in apolipoprotein B100 was one of the first such mutations. Which of the following is an appropriate hypothesis for how apolipoprotein B100 mutations cause hypercholesterolemia?

Which type of cell–cell interaction is responsible for maintaining the correct localization of glucose transporters in polarized intestinal epithelial cells?

A mutation in an epithelial cell leads to the expression of β4 integrin with a deleted cytoplasmic domain. How would this mutation affect adhesion of epithelial cells to basal laminae?

Which of the following is not one of the functions of the cytoskeleton?

Which statement about ion channels is true?

Chitin is a linear polymer of?