Description
Jasplakinolide is a natural macrocyclic peptide first isolated from a marine sponge. It potently inhibits the proliferation of PC3 prostate carcinoma cells (IC
50 = 35 nM) by binding F-
actin (KD = 15 nM). This binding of jasplakinolide to actin, which is competitive with phalloidin, stabilizes actin filaments
in vitro but disrupts actin filaments and induces irregular polymerization of monomeric actin
in vivo. This compound is used to investigate the role of actin in diverse cellular roles, such as motility, transport, and development.
Uses
Jasplakinolide is a natural macrocyclic peptide first isolated from a marine sponge. It potently inhibits the proliferation of PC3 prostate carcinoma cells (IC50 = 35 nM) by binding F-actin (KD = 15 nM). This binding of jasplakinolide to actin, which is competitive with phalloidin, stabilizes actin filaments in vitro but disrupts actin filaments and induces irregular polymerization of monomeric actin in vivo. This compound is used to investigate the role of actin in diverse cellular roles, such as motility, transport, and development.
Uses
Jasplakinolide is a potent inhibitor of prostrate and breast carcinoma cell proliferation. Also acts as an actin stabilizing agent, affecting chromosome movement in studies.
Uses
Jasplakinolide has been used to analyze its influence on sciatic nerve guidance effect
in vivo in chicken embryos. It has also been used to apply on the control cells for the treatment for blocking actin dynamics.
Definition
ChEBI: A cyclodepsipeptide isolated from Jaspis splendens and has been shown to exhibit antineoplastic activity.
Biochem/physiol Actions
Jasplakinolide is an actin-specific reagent that promotes actin polymerization and stabilizes actin filaments. In vitro, Jasplakinolidet potently induces actin polymerization by stimulating actin filament nucleation and competes with phalloidin for actin binding (Kd = 15 nM). In vivo, Jasplakinolide has been found to disrupt actin filaments and induce polymerization of monomeric actin into amorphous masses, the exact mechanism of which has not been determined yet. Jasplakinolide differs from other actin stabilizers in that it is cell permeable. This peptide has fungicidal, insecticidal and antiproliferative activity, and is useful for investigating cell processes mediated by actin polymerization and depolymerization, such as cell adhesion, locomotion, endocytosis, and vesicle sorting and release.
References
[1] M R BUBB. Jasplakinolide, a cytotoxic natural product, induces actin polymerization and competitively inhibits the binding of phalloidin to F-actin.[J]. The Journal of Biological Chemistry, 1994, 269 21: 14869-14871.
[2] M R BUBB. Effects of jasplakinolide on the kinetics of actin polymerization. An explanation for certain in vivo observations.[J]. The Journal of Biological Chemistry, 2000, 275 7: 5163-5170. DOI:
10.1074/jbc.275.7.5163[3] DAVID VAN GOOR. The role of actin turnover in retrograde actin network flow in neuronal growth cones.[J]. PLoS ONE, 2012: e30959. DOI:
10.1371/journal.pone.0030959[4] XIAOYUN ZHANG. Actin stabilization by jasplakinolide affects the function of bone marrow-derived late endothelial progenitor cells.[J]. PLoS ONE, 2012: e50899. DOI:
10.1371/journal.pone.0050899[5] TANJA EISEMANN. An advanced glioma cell invasion assay based on organotypic brain slice cultures.[J]. BMC Cancer, 2018: 103. DOI:
10.1186/s12885-018-4007-4
