The involvement of RNA and protein synthesis in programmed cell death (apoptosis) in human leukaemia HL-60 cells

Martin, Séamus J.; Bonham, Áine M.; Cotter, Thomas G.

doi:10.1042/bst0180634

Cited by 16 publications

(5 citation statements)

References 2 publications

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“…The idea that stalling of translation may provoke the onset of apoptosis in not new ; earlier studies have reported that cells undergoing apoptosis displayed a rapid decrease in protein synthesis. (76)(77)(78)(79) Further, cells could be induced to undergo apoptosis when treated with inhibitors of protein synthesis. (77,80) Indeed, recent studies have also pointed to translational control of apoptosis.…”

Section: Cross-talk Between Translation Initiation and Apoptosismentioning

confidence: 99%

The Emerging Role of the Interferon-Induced PKR Protein Kinase as an Apoptotic Effector: A New Face of Death?

Tan¹,

Katze²

1999

Journal of Interferon & Cytokine Research

104

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Recent research has thrown a spotlight on the interferon (IFN)-induced PKR protein kinase, implicating it as an important effector of apoptosis induced by several cellular stress conditions, including viral infection, cytokine treatment, and growth factor deprivation. In this review, we summarize the evidence for the role of PKR as a death accomplice and discuss how PKR might promote cell demise in light of current knowledge of the molecular mechanisms of apoptosis. Given its new found role and its established antiviral function, it is no wonder that PKR is a popular target for viral evasion of the host defense. PKR-dependent apoptosis may offer a novel cell-death pathway for specific manipulation in therapeutic strategies against apoptosis-related diseases.

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Section: Cross-talk Between Translation Initiation and Apoptosismentioning

confidence: 99%

The Emerging Role of the Interferon-Induced PKR Protein Kinase as an Apoptotic Effector: A New Face of Death?

Tan¹,

Katze²

1999

Journal of Interferon & Cytokine Research

104

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“…Another indication that DNA fragmentation is important is that it occurs very early in the apoptotic process, first appearing several hours before cell viability starts to decrease (49,80,113,114). Another indication that DNA fragmentation is important is that it occurs very early in the apoptotic process, first appearing several hours before cell viability starts to decrease (49,80,113,114).…”

Section: A Chromatin Degradationmentioning

confidence: 99%

“…When chromatin is isolated from thymocytes of glucocorticoid-treated rats and analyzed by agarose gel electrophoresis, DNA degradation is first apparent 2 h after hormone treatment whereas thymocyte viability does not start to decrease until 8 h after treatment. low pH, heating, freeze/thawing, complement, azide, ethanol), the DNA is either not fragmented or is nonspecifically degraded into a continuous spectrum of sizes (113,114,119). Apoptosis and DNA degradation in several cell types are inhibited by the presence of zinc (Zn 2+ ) (115)(116)(117).…”

Section: A Chromatin Degradationmentioning

confidence: 99%

Apoptosis: The Biochemistry and Molecular Biology of Programmed Cell Death*

1993

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“…Another distinction between necrotic and apoptotic cells is the requirement for new mRNA and protein expression during the early stages of some forms of apoptosis (restricted to specific cell types and stimuli). Apoptotic responses that help regulate immune defenses are most often associated with mRNA and protein synthesis (14,16,17,26,27). The nature of the stimuli that triggers cell death, e.g.…”

Section: Historical Introductionmentioning

confidence: 99%

Proteolytic Activities That Mediate Apoptosis

Kidd

1998

Annu. Rev. Physiol.

255

160

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Since the discovery that cells can activate their own suicide program, investigators have attempted to determine whether the events that are associated with this form of cell death are genetically determined. The discovery that the ced-3 gene of Caenorhabditis elegans encodes a cysteine protease essential for developmentally regulated apoptosis ignited interest in this area of research. As a result, we now know that cell death is specified by a number of genes and that this biologic process contributes significantly to development, tumorigenesis, and autoimmune disease. In this review I summarize what is currently known about signaling pathways involved in apoptosis, with particular emphasis on the function of the cysteine proteases known as caspases. However, there is also evidence that protease-independent cell death pathways exist. Is there a relationship between these two distinct mechanisms? If so, how do they communicate? Finally, even though the involvement of tumor necrosis factor/nerve growth factor family of receptors and cysteine proteases has been elegantly established as a component of many apoptotic signaling pathways, what happens downstream of these initial events? Why are only a selected group of cellular proteins-many nuclear-the targets of these proteases? Are nuclear events essential for apoptosis in vivo? Are the cellular genes that encode products involved in apoptotic signaling frequent targets of mutation/alteration during tumorigenesis? These are only a few questions that may be answered in the next ten years.

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The involvement of RNA and protein synthesis in programmed cell death (apoptosis) in human leukaemia HL-60 cells

Cited by 16 publications

References 2 publications

The Emerging Role of the Interferon-Induced PKR Protein Kinase as an Apoptotic Effector: A New Face of Death?

The Emerging Role of the Interferon-Induced PKR Protein Kinase as an Apoptotic Effector: A New Face of Death?

Apoptosis: The Biochemistry and Molecular Biology of Programmed Cell Death*

Proteolytic Activities That Mediate Apoptosis

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