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Related Concept Videos

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While it is unclear how molecules move between adjacent Golgi cisternae, it is apparent that the molecules move from cis- cisterna, the entry face, to the trans- cisterna, the exit face. Experiments initially suggested vesicles that bud from one cisterna and fuse with the next cisterna to transport proteins between the cisternae. This vesicular transport model describes the Golgi apparatus as a relatively static structure with a unique enzyme composition in each cisterna. Molecules are...
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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
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Clathrin-coated vesicles use endocytosis to transport receptors and lysosomal hydrolases from the Golgi to the lysosome in the late secretory pathway. Clathrin-mediated endocytosis was the first described endocytic process, and Clathrin-coated vesicles remain one of the most well-studied transport vesicles. The molecular machinery that generates clathrin-coated vesicles comprises over 50 proteins that precisely coordinate vesicle formation. Cell surface receptors concentrated in indented sites...
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Introduction to Membrane Traffic01:44

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The ER, Golgi apparatus, endosomes, and lysosomes work in tandem to modify, sort, and package proteins and lipids. An integrated membrane trafficking network facilitates the back and forth shuttling of molecules within different organelles in the same cell or across the cell membrane.
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Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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Related Experiment Video

Updated: Jun 16, 2025

SNARE-mediated Fusion of Single Proteoliposomes with Tethered Supported Bilayers in a Microfluidic Flow Cell Monitored by Polarized TIRF Microscopy
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Flow-Induced Vesicle Translocation through a Narrow Slit─Transit Time Scaling Relations.

Bogdan Ranguelov1,2, Peicho Petkov3, Andrey Milchev1

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Langmuir : the ACS Journal of Surfaces and Colloids
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Summary

Vesicle translocation through narrow slits, crucial for drug delivery and microfluidics, was studied. Transit time depends on vesicle size, force, and slit width, with jamming possible at critical forces.

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Area of Science:

  • Soft matter physics
  • Biophysics
  • Nanotechnology

Background:

  • Vesicle and transferosome translocation through splenic interendothelial slits is vital for transdermal drug delivery and microfluidic separations.
  • Understanding these translocation dynamics is key for optimizing drug permeation and disease progression monitoring.

Purpose of the Study:

  • To investigate the pressure-driven flow-induced translocation of loaded vesicles through narrow rectangular slits.
  • To analyze the influence of vesicle size, applied force, and slit geometry on translocation dynamics.

Main Methods:

  • Extensive Molecular Dynamics (MD) simulations were employed.
  • Multiparticle Collision Dynamics (MPCD) was used to incorporate hydrodynamic interactions.
  • Vesicles of varying size (M) were subjected to a constant body force (F) in slits of half-width (H).

Main Results:

  • Transit time (τ) scales as τ ∝ MF⁻¹H⁻², confirming theoretical predictions.
  • A critical jamming force (Fminjam ∝ H⁻¹) was identified, below which vesicles get stuck.
  • At high forces, transit time becomes independent of slit width.
  • Increased internal filler concentration or filler attraction increases vesicle surface area and tension, significantly prolonging transit time.

Conclusions:

  • The study provides a quantitative understanding of vesicle translocation dynamics in confined geometries.
  • Findings are relevant for designing efficient vesicular transdermal delivery systems and advanced microfluidic devices.
  • Vesicle internal properties and surface tension significantly impact translocation efficiency.