Regulation of plasma membrane blebbing by the cytoskeleton

  title={Regulation of plasma membrane blebbing by the cytoskeleton},
  author={J{\"o}rg Hagmann and Max M. Burger and Daniel Dagan},
  journal={Journal of Cellular Biochemistry},
When neuroblastoma cells are exposed to lysophosphatidic acid (LPA), they undergo a vigorous, but transient blebbing phase. The effect is sensitive to inhibition by staurosporine, KT 5926 (an inhibitor of myosin light chain kinase), and cytochalasin B, suggesting that LPA activates the phosphorylation of myosin light chain and increases the contractile activity of the actomyosin network. Cell contractions increase the intracellular pressure driving bleb formation. Calyculin, an inhibitor of… 

Cell motility through plasma membrane blebbing

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Suction pressure can induce uncoupling of the plasma membrane from cortical actin.

The view that blebbing associated with uncoupling of cortical actin and plasma membrane as observed in locomoting cells can be caused by a pressure gradient is supported.

Myosin II–interacting guanine nucleotide exchange factor promotes bleb retraction via stimulating cortex reassembly at the bleb membrane

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Glycogen synthase kinase 3 activation is essential for the snake phospholipase A2 neurotoxin‐induced secretion in chromaffin cells

The results suggest that the activation of this enzyme plays a major role in the enhancement of exocytosis of the readily releasable granules caused by PLA2 neurotoxins in neuroendocrine chromaffin cells.


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Active bleb formation is abated in Lytechinus variegatus red spherule coelomocytes after disruption of acto-myosin contractility.

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Blebbing confers resistance against cell lysis

A previously unknown role for blebbing is disclosed in furnishing resistance to plasmalemmal injury and new therapeutic approaches could be developed to avert the necrotic loss of cells in a variety of human pathologies.

Myosin II-dependent cylindrical protrusions induced by quinine in Dictyostelium: antagonizing effects of actin polymerization at the leading edge.

The results indicate that the force responsible for the quinine-induced protrusion is mainly due to contraction of the cell body, which requires normal myosin II functions, while actin polymerization is important in restricting the direction of its expansion.



Inhibition of lysophosphatidate- and thrombin-induced neurite retraction and neuronal cell rounding by ADP ribosylation of the small GTP-binding protein Rho

RhoA is essential for receptor-mediated force generation and ensuing neurite retraction in N1E-115 and PC12 cells, and that inactivation of RhoA by ADP-ribosylation abolishes actomyosin contractility and promotes neurite outgrowth.

Lysophosphatidic acid induces neuronal shape changes via a novel, receptor-mediated signaling pathway: similarity to thrombin action.

The results indicate that, in N1E-115 and NG108-15 cells, LPA and TRP trigger neurite retraction and cell rounding through a novel, receptor-mediated signaling pathway, and they suggest that p60src may play a role in this pathway.

The architecture of actin filaments and the ultrastructural location of actin-binding protein in the periphery of lung macrophages

A highly branched filament network is the principal structure in the periphery of detergent-extracted cytoskeletons of macrophages that have been spread on a surface and either freeze or critical

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Fibroblast contractility and actin organization are stimulated by microtubule inhibitors.

The silicone rubber substratum technique was used in combination with fluorescence microscopy in order to observe the effects of microtubule-depolymerizing drugs on the contractile strength and organization of cytoplasmic actin networks.

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