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Related Concept Videos

Actin Filament Depolymerization01:19

Actin Filament Depolymerization

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).
In F-actin, the ADF/cofilin proteins...
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Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

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Gelsolin activity controls efficient early HIV-1 infection.

Laura García-Expósito1, Serena Ziglio, Jonathan Barroso-González

  • 1Cellular and Viral Immunology Lab, Department of Physical Medicine and Pharmacology, School of Medicine, University of La Laguna, Campus de Ofra s/n, Tenerife 38071, Spain.

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Summary

Gelsolin controls actin reorganization, acting as a barrier to restrict HIV-1 infection. Manipulating gelsolin levels impacts viral entry and fusion, highlighting its role in limiting infection.

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Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • HIV-1 entry into lymphocytes depends on actin adaptors like moesin and filamin-A for F-actin reorganization.
  • Cortical actin dynamics are crucial for CD4/co-receptor redistribution and membrane tension, facilitating HIV-1 fusion and infection.

Purpose of the Study:

  • To investigate the role of gelsolin in restructuring cortical F-actin during HIV-1 Envelope (Env)-gp120-mediated signaling.
  • To determine if gelsolin dynamics influence HIV-1 fusion, entry, and infection of CD4+ lymphocytes.

Main Methods:

  • Studied gelsolin's effect on cortical F-actin during HIV-1 Env-gp120 signaling.
  • Assessed HIV-1 fusion and infection in lymphocytes with altered gelsolin expression (overexpression and silencing).
  • Analyzed F-actin reorganization, receptor capping, and pseudopodia formation under different gelsolin conditions.

Main Results:

  • Gelsolin restructures cortical F-actin during HIV-1 Env-gp120 signaling without affecting receptor expression or co-receptor signaling.
  • Both gelsolin overexpression and silencing impaired HIV-1 Env-mediated membrane fusion and infection.
  • Gelsolin manipulation disrupted Env-gp120-induced F-actin reorganization, receptor capping, and led to aberrant pseudopodia formation, inhibiting infection.

Conclusions:

  • Gelsolin acts as a barrier restricting HIV-1 infection by severing cortical actin and controlling its availability for reorganization during viral fusion.
  • Gelsolin's role in limiting HIV-1 infection occurs at a pre-fusion step, offering insights into viral entry dynamics.
  • Regulating gelsolin expression or actin-severing activity presents a potential strategy to combat HIV-1 infection.