Endocytosis, exocytosis and vesicles !

Mechanism
For completeness

Cells wrap particles in little membrane bags to bring them in (endocytosis) or to release their contents (exocytosis).

Updated 2026-11-01

Also called: Phagocytosis, Receptor-mediated endocytosis

What it is

Molecules too large for channels or carriers cross the membrane inside vesicles. In endocytosis the membrane folds in and closes around the material; in exocytosis a vesicle fuses with the membrane and empties its contents outside. Both use energy and depend on the cytoskeleton. Ca²⁺-regulated exocytosis is how neurotransmitters, hormones and digestive enzymes are released.

How it works, step by step

A ligand binds its membrane receptor and the complexes gather in a clathrin-coated pit.
The pit folds inwards and dynamin pinches it off: a vesicle forms inside the cell.
The vesicle sheds its clathrin and fuses with an endosome, whose acidic pH separates ligand from receptor.
The receptor returns to the membrane for reuse; the ligand goes on to the lysosome, where hydrolases break it down.
In the reverse route, Golgi vesicles dock at the membrane through SNAREs and, on a Ca²⁺ signal, fuse and release their contents.

Vesicular transport processes

Process	What it moves	Example
Phagocytosis	Large particles (bacteria, dead cells)	Neutrophils and macrophages
Pinocytosis	Extracellular fluid with solutes	Almost all cells
Receptor-mediated endocytosis	Specific ligands	LDL into hepatocytes; transferrin
Transcytosis	Molecules across an epithelium	IgA into the gut lumen; IgG across the placenta
Regulated exocytosis	Granule contents, on demand	Neurotransmitters, insulin, pancreatic enzymes

Clinical notes

Familial hypercholesterolaemia: tendon xanthomas and early coronary disease; heterozygotes are fairly common.
I-cell disease: enzymes miss their mannose-6-phosphate tag, are secreted out of the cell and the lysosome fills with undegraded material.
Botulism: symmetric descending paralysis with dilated pupils, from failed acetylcholine exocytosis.

Test yourself

Think of the answer, then tap the question to see it.

Why is plasma cholesterol high in familial hypercholesterolaemia even though the liver works?

Without a working LDL receptor, receptor-mediated endocytosis fails: LDL cannot enter hepatocytes, stays in plasma, and the liver keeps making cholesterol.

Which step of exocytosis does botulinum toxin block, and what does it cause?

It cleaves SNARE proteins and prevents fusion of acetylcholine vesicles; the result is descending flaccid paralysis.

Why can the LDL receptor be used many times?

The endosome's acidic pH releases LDL from its receptor; the receptor returns to the membrane while LDL goes to the lysosome.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 3.1 The Cell Membrane (OpenStax (Rice University), 2022); 3.2 The Cytoplasm and Cellular Organelles (OpenStax (Rice University), 2022); Familial hypercholesterolemia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 2). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.