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F-actin polymerization in neutrophils describes the rapid assembly of actin filaments (F-actin) from monomeric actin (G-actin) in response to receptor-mediated signals, such as chemoattractant gradients. This cytoskeletal remodeling underlies neutrophil shape change, directional migration (chemo-taxis), and is essential for efficient pathogen clearance by the innate immune system. The process is spatially and temporally regulated by upstream signaling cascades involving G protein-coupled receptors, small Rho-family GTPases (e.g., Cdc42, Rac), phosphoinositide signaling, and actin nucleating factors like the Arp2/3 complex and formins. Modulation of this process is fundamental to both normal immune responses and inflammatory disease pathogenesis.
Inhibition of actin filament elongation (cytochalasins, latrunculins); Stabilization of actin filaments (jasplakinolide); Inhibition of actin nucleation (Arp2/3, formin inhibitors)
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