Transcriptional control of the core cell-death machinery

Kumar, Sharad; Cakouros, Dimitrios

doi:10.1016/j.tibs.2004.02.001

Cited by 68 publications

(63 citation statements)

References 70 publications

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“…Although precisely how dronc expression is regulated is not understood, complex regulation by various transcription factors and chromatin modification/remodelling are likely to contribute to this process. 41 Although DRONC is clearly a caspase which efficiently cleaves synthetic substrates such as VDVAD, and downstream caspases DRICE and DCP-1, following an Asp residue, recombinant DRONC expressed in Escherichia coli can autoprocess following a Glu residue in the P 1 position. 35 This unusual substrate cleavage activity of DRONC may be attributed to an atypical sequence of the catalytic site.…”

Section: Caspasesmentioning

confidence: 99%

“…This could be achieved by increasing the intracellular levels of RPR, HID or GRIM, or by elevating the concentration of DRONC and ARK, the scenarios that are seen during developmental cell death in Drosophila. 41 Loss-of-function mutations in ark block most developmentally programmed cell death, resulting in extra cells in the embryos, hyperplasia of the central nervous system and other abnormalities. [60][61][62] ark mutants essentially phenocopy dronc mutants and show a block in the removal of larval salivary glands, but the histolysis of midgut appears normal in ark-null animals.…”

Section: Activation Of Fly Caspasesmentioning

confidence: 99%

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Caspase function in programmed cell death

2006

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The first proapoptotic caspase, CED-3, was cloned from Caenorhabditis elegans in 1993 and shown to be essential for the developmental death of all somatic cells. Following the discovery of CED-3, caspases have been cloned from several vertebrate and invertebrate species. As reviewed in other articles in this issue of Cell Death and Differentiation, many caspases function in nonapoptotic pathways. However, as is clear from the worm studies, the evolutionarily conserved role of caspases is to execute programmed cell death. In this article, I will specifically focus on caspases that function primarily in cell death execution. In particular, the physiological function of caspases in apoptosis is discussed using examples from the worm, fly and mammals.

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Section: Caspasesmentioning

confidence: 99%

Section: Activation Of Fly Caspasesmentioning

confidence: 99%

Caspase function in programmed cell death

2006

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“…In the fly, HID, Grim, and Reaper are transcriptionally upregulated in response to developmental cues in most cell types; transcriptional upregulation of ARK and DRONC may also be involved in evasion of DIAP1-mediated caspase inhibition. 39 By contrast, in mammalian apoptosis Smac and Omi are released from the mitochondria upon MOMP, along with cytochrome c.…”

Section: Conservation Of a Mitochondrial Role In Cell Death: A Fly Inmentioning

confidence: 99%

Living with death: the evolution of the mitochondrial pathway of apoptosis in animals

2008

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The mitochondrial pathway of cell death, in which apoptosis proceeds following mitochondrial outer membrane permeabilization, release of cytochrome c, and APAF-1 apoptosome-mediated caspase activation, represents the major pathway of physiological apoptosis in vertebrates. However, the well-characterized apoptotic pathways of the invertebrates C. elegans and D. melanogaster indicate that this apoptotic pathway is not universally conserved among animals. This review will compare the role of the mitochondria in the apoptotic programs of mammals, nematodes, and flies, and will survey our knowledge of the apoptotic pathways of other, less familiar model organisms in an effort to explore the evolutionary origins of the mitochondrial pathway of apoptosis.

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“…51,52 In worms and mammals, loss-of-function mutations in the insulin/IGF-1 signalling pathway also antagonise tumour cell growth through activating a p53-mediated cell death pathway. 53 Together, these results implicate the function of tumour suppressor p53 in ageing Figure 2 Autophagy in signalling network of ageing.…”

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confidence: 99%

Autophagy genes and ageing

2008

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Ageing in divergent animal phyla is influenced by several evolutionarily conserved signalling pathways, mitochondrial activity and various environmental factors such as nutrient availability and temperature. Although ageing is a multifactorial process with many mechanisms contributing to the decline, the intracellular accumulation of damaged proteins and mitochondria is a feature common to all aged cells. Autophagy (cellular self-eating) -a lysosome-mediated catabolic process of eukaryotic cells to digest their own constituents -is a major route for the bulk degradation of aberrant cytosolic macromolecules and organelles. Indeed, genetic studies show that autophagy-related genes are required for lifespan extension in various long-lived mutant nematodes and promote survival in worms and flies exposed to prolonged starvation. These data implicate autophagy in ageing control. Furthermore, results in Drosophila demonstrate that promoting basal expression of the autophagy gene Atg8 in the nervous system extends lifespan by 50%, thereby providing evidence that the autophagy pathway regulates the rate at which the tissues age. In this review, the molecular mechanisms by which autophagy genes interact with longevity pathways in diverse organisms ranging from yeast to mammals are discussed.

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Transcriptional control of the core cell-death machinery

Cited by 68 publications

References 70 publications

Caspase function in programmed cell death

Caspase function in programmed cell death

Living with death: the evolution of the mitochondrial pathway of apoptosis in animals

Autophagy genes and ageing

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