Receptor Mediated Endocytosis Flashcards
Is the uncoating of a clathrin coat spontaneous or need ATP?
Needs enzymes which are ATP dependent
How does the formation of a clathrin coat in insulin differ from others?
Clathrn coat only forms when a receptor has a ligand bound
What are the general stages of RME?
Receptors cluster over clathrin, ligand binds causing conformational change, spontaneous constitutive invagination of membrane, forms coated vesicles, ATP dependent uncoating, vesicle fuses with endosome.
What receptors are present for the uptake of cholesterol?
Cells that require cholesterol produce receptors for apoprotein B
When LDL and its receptor reaches an endosome what happens?
The acidity reduces affinity of receptor for LDL TF it dissociates, receptor buds off in own vesicle and is recycled back to membrane. LDL buds off to lysosome. Cholesterol is de-esterified and released into the cell.
What binds to the receptor in the uptake of FE3+?
Transferrin
At what ph does transferrin bind to the receptor?
Neutral
What forms transferrin?
Apotransferring and Fe3+
In the uptake of cholesterol, what happens to the receptor and ligand?
Receptor: recycled. Ligand: degraded.
In the uptake of Fe3+ what happens to the receptor and ligand overall?
Receptor: recycled. Ligand: degraded.
When transferrin and the receptor reach an endosome what happens?
Acidity of the endosome lowers affinity of transferrin for Fe3+, so Fe3+ dissociates leaving behind apotransferrin bound to the receptor.
What happens to the apotransferrin once Fe3+ has dissociated in RME?
Receptor with apotransferrin bound bud off in vesicle and are recycled to membrane. When the extracellular pH drops (more acidic) affinity of receptor for apotransferrin drops and so it dissociates.
What happens in the RME of insulin that is different to others?
In the late endosome, the receptor and insulin remain bound and so both are delivered to the lysosome. Lysosomal enzymes TF degrade both receptor and insulin.
How does the way the RME of insulin work lead to desensitisation of target cells to insulin?
Every time insulin binds, receptor complex is internalised and degraded. (More insulin, more degradation). Rate of synthesis cant keep up, TF overall loss of receptors.
Is the formation of Clathrin spontaneous or need ATP?
Spontaneous