Molecular regulation of apoptosis: Genetic controls on cell death

作者: Gwyn T. Williams , Christopher A. Smith

DOI: 10.1016/0092-8674(93)90457-2

关键词: Second messenger systemCellTumor suppressor geneCell typeProgrammed cell deathStem cellGeneticsIntracellularCell biologyBiologyApoptosis

摘要: Cell death is now a very lively field. The study of active cellular self-destruction through apoptosis (Wyllie et al., 1980) has become much part the mainstream in cell biology, particularly immunology, developmental and oncology. significance process increasingly recognized both physiological regulation pathological situations (reviewed by Williams 1992). As subject been largely neglected for long time, at molecular level, there lot catching up to do. There are few, if any, other generally important aspects behavior where so fundamental work still be done, which makes this interesting field watch. It widely accepted that genedirected can seen, alongside more familiar gene-directed processes like differentiation, as repertoire available respond external internal stimuli (Figure 1). Until recently, most information on genetics programed was derived from studies nematode Caenorhabditis elegans Ellis 1991) but about intracellular signals involved stimulation suppression mammalian cells also emerging. Intracellular Inducers Apoptosis lead probably varied those differentiation proliferation 1992) include withdrawal extracellular well their appearance. Indeed, dependenceon essential survival factors appears widespread Raff, In hemopoietic stem cells, primary function colony-stimulating (Williams 1990) effect allows an intrinsically determined pathway followed (Fairbairn 1993). contrast, some surface molecules, such tumor necrosis factor receptor APO-l antigen (now known identical Fas antigen), often induce apoptosis, although not always outcome (Mapara Several different second messenger systems have associated with induction final response varies type being received. Consequently, addition genes exclusively death, likely Minireview

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