Cytochalasin D (Zygosporin A) is a potent actin polymerization inhibitor, could be derived from fungus. Cytochalasin D has cell-permeable activity. Cytochalasin D inhibits the G-actin–cofilin interaction by binding to G-actin. Cytochalasin D also inhibits the binding of cofilin to F-actin and decreases the rate of both actin polymerization and depolymerization in living cells. Cytochalasin D can reduce exosome release, in turn reducing the amount of survivin present in the tumour environment. Cytochalasin D induces phosphorylation and cytoplasmic retention of Yap.

Solid

Cytochalasin D (3 and 10 μM; 30 min) causes retraction and arborization of COS-7 cells and conversion of F-actin from long fibers to punctate structures.
Cytochalasin D (0.3, 1, 3 and 10 μM; 30 min) concentration-dependently decreases the rate of actin depolymerization in COS-7 cells.
Cytochalasin D (1 μM; NIH3T3 cells) disrupts stress fibers, induces phosphorylation of Yap, while cells maintains original area and lost nuclear Yap localization.

Medlife has not independently confirmed the accuracy of these methods. They are for reference only.

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• [1]. Shoji K, et, al. Cytochalasin D acts as an inhibitor of the actin-cofilin interaction. Biochem Biophys Res Commun. 2012 Jul 20;424(1):52-7.  [Information]

  [2]. Flanagan MD, et, al. Cytochalasins block actin filament elongation by binding to high affinity sites associated with F-actin. J Biol Chem. 1980 Feb 10;255(3):835-8.  [Information]

  [3]. Catalano M, et, al. Inhibiting extracellular vesicles formation and release: a review of EV inhibitors. J Extracell Vesicles. 2019 Dec 19;9(1):1703244.  [Information]

  [4]. Wada K, et, al. Hippo pathway regulation by cell morphology and stress fibers. Development. 2011 Sep;138(18):3907-14.  [Information]

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