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Death-associated protein kinase (DAPK) regulates many distinct signalling events, including apoptosis, autophagy and membrane blebbing. The role of DAPK in the blebbing process is only beginning to be understood and, in this review, we will first summarize what is known about the cytoskeletal proteins and signalling cascades that participate in bleb growth and retraction and then highlight how DAPK integrates with these processes. Membrane blebs are quasispherical cellular protrusions that have a lifetime of approximately 2 min. During expansion, blebs are initially devoid of actin, although actomyosin contractions provide the motive force for growth. Once growth slows, an actin cortex reforms and actin-bundling and contractile proteins are recruited. Finally, myosin contraction powers bleb retraction into the cell body. Blebbing occurs in a variety of cell types, from cancerous cells to embryonic cells, and can be seen in cellular phenomena as diverse as cell spreading, movement, cytokinesis and cell death. Although the machinery that executes this is still undefined in detail, the conservation of blebbing phenomenon suggests a fundamental role in metazoans and DAPK offers a door to further dissect this fascinating process.

Original publication

DOI

10.1111/j.1742-4658.2009.07412.x

Type

Journal article

Journal

Febs j

Publication Date

01/2010

Volume

277

Pages

58 - 65

Keywords

Actomyosin, Animals, Apoptosis, Apoptosis Regulatory Proteins, Autophagy, Calcium-Calmodulin-Dependent Protein Kinases, Cell Surface Extensions, Death-Associated Protein Kinases, Humans, Models, Biological, Signal Transduction