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Review
. 1999 Aug 23;146(4):703-8.
doi: 10.1083/jcb.146.4.703.

Extranuclear apoptosis. The role of the cytoplasm in the execution phase

Affiliations
Review

Extranuclear apoptosis. The role of the cytoplasm in the execution phase

J C Mills et al. J Cell Biol. .
No abstract available

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Figures

Figure 1
Figure 1
Scheme for temporal and mechanistic organization of the cytoplasmic execution phase. (Top) Morphological view. (Bottom) Corresponding actin rearrangements.
Figure 2
Figure 2
Model for bleb extrusion. Contraction of cortical actin filaments by myosin II causes contraction of plasma membrane, except in focal regions of weakness in actin links to the membrane. Such regions of weakness can be caused by cleavage of membrane-anchoring proteins (e.g., fodrin). The combination of contraction and focal loss of membrane support leads to bleb formation.
Figure 3
Figure 3
Possible altruistic role of apoptosis in epithelial cells. The same actomyosin contractile forces that cause blebbing can pull neighboring cells to cover potential gaps in the monolayer and maintain barrier function.

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References

    1. Bannerman D.D., Sathyamoorthy M., Goldblum S.E. Bacterial lipopolysaccharide disrupts endothelial monolayer integrity and survival signaling events through caspase cleavage of adherens junction proteins. J. Biol. Chem. 1998;273:35371–35380. - PubMed
    1. Brancolini C., Lazarevic D., Rodrigquez J., Schneider C. Dismantling cell-cell contacts during apoptosis is coupled to a caspase-dependent proteolytic cleavage of β-catenin. J. Cell Biol. 1997;139:759–771. - PMC - PubMed
    1. Cardone M.H., Salvesen G.S., Widmann C., Johnson G., Frisch S.M. The regulation of anoikisMEKK-1 activation requires cleavage by caspases. Cell. 1997;90:315–323. - PubMed
    1. Cotter T.G., Lennon S.V., Glynn J.M., Green D.R. Microfilament disrupting agents prevent the formation of apoptotic bodies in tumor cells undergoing apoptosis. Cancer Res. 1992;52:997–1005. - PubMed
    1. Cryns V.L., Bergeron L., Zhu H., Li H., Yuan J. Specific cleavage of alpha-fodrin during Fas- and tumor necrosis factor-induced apoptosis is mediated by an interleukin-1 beta-converting enzyme/Ced-3 protease distinct from the poly(ADP-ribose) polymerase protease. J. Biol. Chem. 1996;271:31277–31282. - PubMed