Cytochalasin B
Actin filament disrupting agent / A cell permeable fungal toxin which binds to the barbed end of actin, inhibiting its polymerization.1 Inhibits cell division, migration and glucose transport.2 Causes cell cycle arrest at G2/M and induces apoptosis in HCT-116 colorectal carcinoma cells.3 Cytochalasin B-induced membrane vesicles (CIMVs) retain cell surface receptors of the parent cells and retain fusion specificity with target cells.4 CIMVs are a promising new vector system for drug and biomolecule delivery due to their natural origin and participation in intercellular communication.5
Biochemicals & reagents
14930-96-2
NSC107658; Phominone; Phomin
1) Threadoropoulos et al. (1994), Cytochalasin B may shorten actin filaments by a mechanism independent of barbed end capping; Biochem. Phramcol., 47 1875 2) Whitesell et al. (2005), Compartmentalization of transport and phosphorylation of glucose in a hepatoma cell line; Biochem. J., 386 245 3) Buldak et al. (2014), changes in subcellular localization of visfatin in human colorectal HCT-116 carcinoma cell line after cytochalasin B treatment; Eur. J. Histochem., 58 2408 4) Gomzikova et al. (2018), Evaluation of cytochalasin B-Induced Membrane Vesicles Fusion specificity with Target Cells; Biomed. Res. Int., 2018 7053623 5) Gomzikova et al. (2017), Cytochalasin B-induced membrane vesicles convey angiogenic activity of parental cells; Oncotarget, 8 70496
-20°C
TARGET: Cytoskeleton -- PATHWAY: Cell cycle; Glucose metabolism; Intracellular transport; Apoptosis inducer; Cell migration -- RESEARCH AREA: Cell death; Vesicles; Angiogenesis -- DISEASE AREA: Cancer