Franklin-Tong, V.E. and Gourlay, C.W. (2008) A role for actin in regulating apoptosis/programmed cell death: evidence spanning yeast, plants and animals. Biochemical Journal, 413 (3). pp. 389-404. ISSN 0264-6021 .
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Achieving an understanding of how apoptosis/PCD (programmed cell death) is integrated within cellular responses to environmental and intracellular signals is a daunting task. From the sensation of a stimulus to the point of no return, a programme of cell death must engage specific pro-death components, whose effects can in turn be enhanced or repressed by downstream regulatory factors. In recent years, considerable progress has been made in our understanding of how components involved in these processes function. We now know that some of the factors involved in PCD networks have ancient origins that pre-date multicellularity and, indeed, eukaryotes themselves. A subject attracting much attention is the role that the actin cytoskeleton, itself a cellular component with ancient origins, plays in cell death regulation. Actin, a key cellular component, has an established role as a cellular sensor, with reorganization and alterations in actin dynamics being a well known consequence of signalling. A range of studies have revealed that actin also plays a key role in apoptosis/PCD regulation. Evidence implicating actin as a regulator of eukaryotic cell death has emerged from studies from the Animal, Plant and Fungal Kingdoms. Here we review recent data that provide evidence for an active, functional role for actin in determining whether PCD is triggered and executed, and discuss these findings within the context of regulation of actin dynamics.
|Uncontrolled keywords:||actin, apoptosis, mitochondrion, programmed cell death (PCD), reactive oxygen species (ROS).|
|Subjects:||Q Science > QH Natural history > QH301 Biology|
|Divisions:||Faculties > Science Technology and Medical Studies > School of Biosciences|
|Depositing User:||Campbell Gourlay|
|Date Deposited:||01 Oct 2009 08:46|
|Last Modified:||30 May 2012 08:55|
|Resource URI:||http://kar.kent.ac.uk/id/eprint/22637 (The current URI for this page, for reference purposes)|
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