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Generation of Straight or Branched Actin Filaments01:14

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The straight or branched structure formation of actin filaments is controlled by nucleating proteins such as the formins and Arp2/3 complex. Formin-mediated assembly results in straight filaments, whereas Arp2/3 protein complex-mediated assembly results in branched actin filaments.
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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
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Tension Response at Adherens Junctions01:26

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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
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Updated: Oct 22, 2025

Equibiaxial Stretching Device for High Magnification Live-Cell Confocal Fluorescence Microscopy
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BRAF Modulates Stretch-Induced Intercellular Gap Formation through Localized Actin Reorganization.

Anna Hollósi1, Katalin Pászty1, Miklós Kellermayer1

  • 1Department of Biophysics and Radiation Biology, Semmelweis University, H-1094 Budapest, Hungary.

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Mechanical stretch disrupts endothelial cell barriers by forming gaps. BRAF knockdown prevents this, stabilizing cell junctions and restoring barrier function, offering therapeutic potential for conditions like high blood pressure.

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Area of Science:

  • Cell Biology
  • Biophysics
  • Physiology

Background:

  • Endothelial cell-cell adhesion is crucial for barrier function.
  • Mechanical forces actively remodel the actin cytoskeleton to maintain cell junctions.
  • The role of BRAF in endothelial response to mechanical stress is not fully understood.

Purpose of the Study:

  • To investigate the role of BRAF in the endothelial cell response to mechanical stretch.
  • To determine how BRAF influences actin cytoskeleton organization and cell-cell adhesion under stress.
  • To assess the potential of BRAF modulation to restore endothelial barrier function.

Main Methods:

  • Mechanical stretch applied to endothelial monolayers.
  • BRAF knockdown using RNA interference (RNAi).
  • Analysis of actin cytoskeleton organization and intercellular gap formation.

Main Results:

  • Control cells formed actin cables and intercellular gaps upon stretching.
  • BRAF knockdown prevented gap formation and stabilized cell junctions.
  • BRAF-deficient cells exhibited excessive stress fiber formation.
  • BRAF RNAi reverted stretch-induced gap formation and restored barrier function.

Conclusions:

  • BRAF plays a critical role in regulating endothelial barrier function under mechanical stress.
  • BRAF modulates actin cytoskeleton dynamics in response to external forces.
  • Targeting BRAF offers a potential strategy to prevent or treat conditions involving endothelial barrier dysfunction due to mechanical stress.