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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...
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
Assembly of Cytoskeletal Filaments01:18

Assembly of Cytoskeletal Filaments

Cytoskeletal filaments are polymeric forms of smaller protein subunits. However, individual cytoskeletal filaments may easily disassemble or associate with other similar filaments to form rigid structures. Microfilaments, made of actin monomers, rely on actin-binding proteins to form bundles and create networks of individual actin filaments. Microtubules rely on microtubule-associated proteins (MAPs) to form sturdy cylindrical structures. However, the proteins involved in forming complex...
Generation of Straight or Branched Actin Filaments01:14

Generation of Straight or Branched Actin Filaments

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.
Arp2/3 Complex
Arp2/3 complex is a seven-subunit complex consisting of two proteins similar to actin- Arp2 and Arp3, and five other subunits that help keep Arp2 and Arp3 inactive. When required, the complex is...
Adaptability of Cytoskeletal Filaments01:12

Adaptability of Cytoskeletal Filaments

The cytoskeleton is a complex dynamic structure performing varied functions based on cellular requirements. The adaptability of the individual filaments in the cytoskeleton determines their ability to perform various functions within the cell. It can undergo rapid reorganization during processes like cell division or remain stable for several hours as in the interphase. The adaptability of these filaments depends on stringent regulatory mechanisms. The microfilament and microtubules of the...
Formation of Intermediate Filaments00:57

Formation of Intermediate Filaments

Intermediate filaments are cytoskeletal proteins with higher tensile strength and flexibility than microfilaments and microtubules. Unlike the other two cytoskeletal proteins, intermediate filament formation lacks the enzymatic activity to hydrolyze nucleotides like ATP and GTP to generate energy for polymerization. Therefore, the formation of intermediate filaments is multistep self-assembly. The involvement of any accessory proteins in intermediate filament formation has not yet been reported.

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Related Experiment Video

Updated: Jun 30, 2026

Aip1p Dynamics Are Altered by the R256H Mutation in Actin
08:57

Aip1p Dynamics Are Altered by the R256H Mutation in Actin

Published on: July 30, 2014

How to engage Cofilin.

Michael Bukrinsky1

  • 1George Washington University, Department of Microbiology, Immunology and Tropical Medicine, Washington, DC 20037, USA. mtmmib@gwumc.edu

Retrovirology
|September 24, 2008
PubMed
Summary
This summary is machine-generated.

Human immunodeficiency virus (HIV) exploits resting CD4+ T cells by activating cofilin, which disrupts actin barriers. This viral mechanism facilitates HIV replication in latent reservoirs, hindering curative therapies.

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Related Experiment Videos

Last Updated: Jun 30, 2026

Aip1p Dynamics Are Altered by the R256H Mutation in Actin
08:57

Aip1p Dynamics Are Altered by the R256H Mutation in Actin

Published on: July 30, 2014

Imaging Intranuclear Actin Rods in Live Heat Stressed Drosophila Embryos
07:57

Imaging Intranuclear Actin Rods in Live Heat Stressed Drosophila Embryos

Published on: May 15, 2020

Using Microfluidics and Fluorescence Microscopy to Study the Assembly Dynamics of Single Actin Filaments and Bundles
08:02

Using Microfluidics and Fluorescence Microscopy to Study the Assembly Dynamics of Single Actin Filaments and Bundles

Published on: May 5, 2022

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Resting CD4+ T cells harbor latent human immunodeficiency virus (HIV), serving as a viral reservoir.
  • This reservoir is a primary obstacle to curative HIV drug therapies.
  • Mechanisms regulating HIV replication in resting T cells remain incompletely understood.

Purpose of the Study:

  • To elucidate novel mechanisms of HIV replication in resting T cells.
  • To identify key viral and cellular interactions driving HIV latency.
  • To explore potential therapeutic targets for combating HIV reservoirs.

Main Methods:

  • Analysis of viral entry pathways in resting CD4+ T cells.
  • Investigation of signaling cascades initiated by HIV gp120-CXCR4 interaction.
  • Assessment of cofilin activity and actin dynamics during viral infection.

Main Results:

  • HIV entry into resting T cells triggers a signaling cascade via gp120-CXCR4.
  • This interaction activates cofilin, a key regulator of actin polymerization.
  • Cofilin activation leads to actin depolymerization, breaching a natural barrier to HIV replication.

Conclusions:

  • HIV employs a novel strategy to infect resting CD4+ T cells by manipulating actin dynamics.
  • Targeting the gp120-CXCR4-cofilin pathway could offer new anti-HIV therapeutic strategies.
  • Understanding these mechanisms is crucial for developing strategies to eradicate latent HIV reservoirs.