Flashcards in Receptor-Mediated Endocytosis Deck (10):
Internalisation of particulate matter via a zipper mechanism
Invagination of the membrane to permit the uptake of extracellular solutes
Selective internalisation of molecules into cells by binding specific cell surface receptors
Describe cholesterol uptake into cells by receptor-mediated endocytosis
LDLs have apoB which is an address protein.
Receptors are at clathrin coated pits, which form spontaneously, as does internalisation.
The coat stops membrane fusion so must be uncoated by an ATP-dependent uncoating protein.
Describe the defects that may be present in the membrane to cause hypocholesterolaemia
The LDL binding site may be defective, or the LDL is able to bind normally with the receptors away from a clathrin coated pit so they are unable to be endocytosed
Describe how endocytosed LDL releases cholesterol.
The uncoated vesicle fuses with an endosome.
This is more acidic due to an ATP-dependent H+ pump.
The low pH lowers the affinity for the receptor/ligand. The receptor remains in the membrane.
The ligand enters a lysosome where it's digested to release cholesterol esters.
Receptor vesicles bud off and are recycled.
Describe how transferrin allows iron uptake into a cell, including the process of removing iron once in the cell.
Apotransferrin binds to iron, becoming ferrotransferrin.
This binds to a receptor for uptake into the cell. Iron is released in the endosome, and the transferrin is recycled to the surface with the receptor.
This is because apot has a high affinity for the receptor when Fe3+ is bound or at pH7.
Describe how immunoglobin is taken up and excreted in bile from hepatocytes
The Ig receptor remains bound in the endosome, vesicles bud off to transfer vesicles which bind to the bile canaliculi.
Cleavage of the receptor removes the antibody and some receptor.
This also occurs in the placenta.
Describe how downregulation of the insulin response can lead to type 2 diabetes mellitus
When insulin and its receptor are taken up in a cell they are both digested, desensitising the cell.
When a person has basal hyperinsulinaemia, cells become persistently desensitised which makes hepatocytes think that the body is starving so they produce more glucose, leading to hyperglycaemia which exacerbates the original effect.
The cycle continues, making it harder to produce insulin.
Beta cells are sensitive and start to die when they are overwhelmed, leading to T2DM