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F-actin podosome (None established; "podosome" is the standard term.)

Target
None established; "podosome" is the standard term.
Molecular classification
Other (subcellular cytoskeletal structure), Actin-based cellular protrusion
01

Overview

A **podosome** is a dynamic conical subcellular structure found on the plasma membrane surface in various animal cells including macrophages, dendritic cells, osteoclasts, endothelial cells, and megakaryocytes. Its defining feature is an **F-actin–rich core**, surrounded by an adhesive ring composed mainly of integrins and associated linker/scaffold proteins such as talin and vinculin. Podosomes mediate key functions including cell–matrix adhesion, extracellular matrix degradation/remodeling for tissue invasion/migration processes, mechanosensing/probing their environment via force generation from continuous actin polymerization within their core. Their architecture includes both lateral/dorsal unbranched actins connecting adjacent cores/rings and regulatory modules controlling contractility. While essential for physiological processes like immune surveillance/migration and bone resorption via osteoclasts' sealing zones during bone remodeling/resorption events,[1][2] aberrant regulation may contribute to pathological states such as cancer metastasis through related structures called invadopodia.[1][2][3]

Other names
PodosomeActin-rich adhesion structure
02

Mechanism of action

For agents that affect these structures: - Inhibition of actin polymerization prevents formation and function of the F-actin core within podosomes, thereby blocking cell migration/invasion capabilities mediated by these structures. - Disruption/modulation of integrins or associated signaling can impair ring complex assembly.

03

Biological functions

Cell–matrix adhesionExtracellular matrix degradation/remodelingMechanosensing/mechanical probing of environmentCell migration and invasionCellular fusion (notably in osteoclasts)
04

Disease associations

Cancer (via related structures called invadopodia in invasive cancer cells)Bone diseases (osteoclast function and bone resorption)Inflammation/immune response modulation (macrophages, dendritic cells)
05

Safety considerations

Not applicable directly—since this is not a direct drug target—but disruption could theoretically impair normal immune cell migration, bone remodeling, or wound healing if targeted systemically.
06

Interacting drugs

Cytochalasin D

3 more in the full profile.

07

Biomarkers

F-actinTks5WASP/WIPCortactinArp2/3 complex proteins

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