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Published on: October 20, 2014
Frustrated clathrin-mediated endocytosis - causes and possible functions
Francesco Baschieri1, Kseniia Porshneva2, Guillaume Montagnac1
1Inserm U1279, Gustave Roussy Institute, Université Paris-Saclay, Villejuif 94805, France guillaume.montagnac@gustaveroussy.fr francesco.baschieri@gustaveroussy.fr.
Frustrated endocytosis, where clathrin-coated structures struggle to bend membranes, is not a failure but serves crucial cellular functions. This review explores its causes and roles in cell physiology and disease.
Area of Science:
- Cell Biology
- Molecular Biology
Background:
- Clathrin-mediated endocytosis is vital for cellular uptake of receptors and ligands.
- Clathrin-coated structures normally cluster receptors and bend membranes to form vesicles.
- Recent findings reveal that membrane deformation by these structures can be impaired.
Purpose of the Study:
- To provide a historical perspective on frustrated endocytosis.
- To define frustrated endocytosis within the clathrin pathway in mammalian cells.
- To discuss the causes and functional consequences of frustrated endocytosis.
Main Methods:
- Literature review of existing research on clathrin-mediated endocytosis.
- Analysis of studies investigating impaired membrane bending and budding.
- Synthesis of findings on the cellular roles of frustrated endocytosis.
Main Results:
- Frustrated endocytosis occurs when environmental or genetic factors impede membrane bending/budding.
- This impaired process is increasingly recognized for its specific cellular functions, not just as a passive outcome.
- The review highlights potential roles in both normal physiology and disease states.
Conclusions:
- Frustrated endocytosis represents a significant cellular response to physical constraints on membrane dynamics.
- Understanding this phenomenon is crucial for comprehending cell physiology and disease mechanisms.
- Further research into frustrated endocytosis could reveal novel therapeutic targets.
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