Tissue Transglutaminase: A Candidate Effector Element of Physiological Cell Death
The metazoans possess a genetic program of cell death (defined morphologically as apoptosis) which plays a vital role in their development and maintainance of tissue homeostasis (Wyllie et al. 1980; Fesus et al. 1991b). Over the last few years, it has become clear that cells not only control their proliferative and differentiative pathways, but also need specific positive stimuli to survive (Fesus et al. 1991 b; Raff et al. 1992). In the absence of the appropriate survival signals, cells enter an active program of cell death which requires the participation of functionally distinct sets of genes (Arends and Wyllie 1991; Fesus et al. 1991b). Despite its widespread importance, little is yet known about the biochemical events leading to the physiological deletion of cells in tissues (Arends and Wyllie 1991; Fesus et al. 1991b). While the mechanisms of initiation and regulation of apoptosis have attracted the attention of many researchers, by far less interest has been focused on the effector genes that determine the irreversible phenotypical changes and clearance of the dying cells. These final events allows naturally occurring cell death to behave as a “social” phenomenon which does not produce damage or inflammation in tissues (Arends and Wyllie 1991; Fesus et al. 1991b). Several independent laboratories have shown tissue transglutaminase (tTG) to be a potentially important player in the last stage of the cell death program (for review see Piacentini et al. 1994).
KeywordsLysine Histamine Dexamethasone Prostaglandin Glucocorticoid
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