(-)-Blebbistatin

Non-muscle myosin II (NM II) ATPase inhibitor

(-)-Blebbistatin

Non-muscle myosin II (NM II) ATPase inhibitor

From: 287 USD
Catalog #
(Select a product)
Non-muscle myosin II (NM II) ATPase inhibitor
Add to Wish List

Overview

(-)-Blebbistatin is a selective cell-permeable inhibitor of non-muscle myosin II ATPases (Kovács et al.; Straight et al.).  It rapidly and reversibly inhibits Mg-ATPase activity and in vitro motility of non-muscle myosin IIA and IIB for several species (IC₅₀ = 0.5-5.0 μM), while poorly inhibiting smooth muscle myosin (IC₅₀ = 80 μM) (Limouze et al.).

MAINTENANCE AND SELF-RENEWAL
· Increases human pluripotent stem cell (hPSC) survival and cloning efficiency after dissociation to single cells, downstream of ROCK inhibition (Chen et al.; Ohgushi et al.; Walker et al.; Xu et al.).
· Enables hPSC to be cultured on microcarriers without surface coating (Chen et al.)
· Inhibits differentiation of human mesenchymal stem cells (McBeath et al.; Engler et al.).
Cell Type
Mesenchymal Stem and Progenitor Cells, Pluripotent Stem Cells
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Maintenance
Area of Interest
Stem Cell Biology
CAS Number
856925-71-8
Chemical Formula
C₁₈H₁₆N₂O₂
Purity
≥ 98%
Target
NM II ATPase

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
(-)-Blebbistatin
Catalog #
72404, 72402
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
(-)-Blebbistatin
Catalog #
72404, 72402
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (10)

Revealing a core signaling regulatory mechanism for pluripotent stem cell survival and self-renewal by small molecules. Xu Y et al. Proceedings of the National Academy of Sciences of the United States of America 2010 MAY

Abstract

Using a high-throughput chemical screen, we identified two small molecules that enhance the survival of human embryonic stem cells (hESCs). By characterizing their mechanisms of action, we discovered an essential role of E-cadherin signaling for ESC survival. Specifically, we showed that the primary cause of hESC death following enzymatic dissociation comes from an irreparable disruption of E-cadherin signaling, which then leads to a fatal perturbation of integrin signaling. Furthermore, we found that stability of E-cadherin and the resulting survival of ESCs were controlled by specific growth factor signaling. Finally, we generated mESC-like hESCs by culturing them in mESC conditions. And these converted hESCs rely more on E-cadherin signaling and significantly less on integrin signaling. Our data suggest that differential usage of cell adhesion systems by ESCs to maintain self-renewal may explain their profound differences in terms of morphology, growth factor requirement, and sensitivity to enzymatic cell dissociation.
Non-muscle myosin II regulates survival threshold of pluripotent stem cells. Walker A et al. Nature communications 2010 JAN

Abstract

Human pluripotent stem (hPS) cells such as human embryonic stem (hES) and induced pluripotent stem (hiPS) cells are vulnerable under single cell conditions, which hampers practical applications; yet, the mechanisms underlying this cell death remain elusive. In this paper, we demonstrate that treatment with a specific inhibitor of non-muscle myosin II (NMII), blebbistatin, enhances the survival of hPS cells under clonal density and suspension conditions, and, in combination with a synthetic matrix, supports a fully defined environment for self-renewal. Consistent with this, genetically engineered mouse embryonic stem cells lacking an isoform of NMII heavy chain (NMHCII), or hES cells expressing a short hairpin RNA to knock down NMHCII, show greater viability than controls. Moreover, NMII inhibition increases the expression of self-renewal regulators Oct3/4 and Nanog, suggesting a mechanistic connection between NMII and self-renewal. These results underscore the importance of the molecular motor, NMII, as a novel target for chemically engineering the survival and self-renewal of hPS cells.
Molecular pathway and cell state responsible for dissociation-induced apoptosis in human pluripotent stem cells. Ohgushi M et al. Cell stem cell 2010 AUG

Abstract

Human embryonic stem cells (hESCs), unlike mouse ones (mESCs), are vulnerable to apoptosis upon dissociation. Here, we show that the apoptosis, which is of a nonanoikis type, is caused by ROCK-dependent hyperactivation of actomyosin and efficiently suppressed by the myosin inhibitor Blebbistatin. The actomyosin hyperactivation is triggered by the loss of E-cadherin-dependent intercellular contact and also observed in dissociated mouse epiblast-derived pluripotent cells but not in mESCs. We reveal that Abr, a unique Rho-GEF family factor containing a functional Rac-GAP domain, is an indispensable upstream regulator of the apoptosis and ROCK/myosin hyperactivation. Rho activation coupled with Rac inhibition is induced in hESCs upon dissociation, but not in Abr-depleted hESCs or mESCs. Furthermore, artificial Rho or ROCK activation with Rac inhibition restores the vulnerability of Abr-depleted hESCs to dissociation-induced apoptosis. Thus, the Abr-dependent Rho-high/Rac-low" state plays a decisive role in initiating the dissociation-induced actomyosin hyperactivation and apoptosis in hESCs."