Induction of tumor necrosis factor synthesis in human monocytes treated by transcriptional inhibitors

Voitenok, Nikolai N.; Misuno, Natalia I.; Panyutich, Alexander V.; Kolesnikova, T. S.

doi:10.1016/0165-2478(89)90072-2

Cited by 12 publications

(5 citation statements)

References 6 publications

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“…In addition, in the case of TNF it has been shown that macrophages in the presence of ActD released increased amounts of TNF spontaneously and upon stimulation with endotoxin. 63 ,M We found that LPS stimulated the subsequent release of TNF from murine Kupffer cells (l0 ngll 0' macrophages after 5 hours) up to 30 minutes after preincubation with AnD. An explanation for these observations may be a posttranscriptional regulation of TNF synthesis.…”

Section: Discussionmentioning

confidence: 75%

Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

et al. 1997

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Section: Discussionmentioning

confidence: 75%

Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

et al. 1997

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“…Meanwhile, it was also reported that the drug induces upregulation of tumor necrosis factor (TNF), which leads to apoptosis [122,123]. The mechanism inducing cell death after transcriptional repression was not clarified, and we do not know exactly what kinds of effects are induced by transcriptional repression.…”

Section: Transcriptional Repression Causes Neuronal Dysfunction and Dmentioning

confidence: 98%

Polyglutamine diseases: a transcription disorder?

Okazawa¹

2003

Cellular and Molecular Life Sciences (CMLS)

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Various molecular processes including unfolded protein response, protein transport, synaptic transmission and transcription are implicated in the pathology of polyglutamine diseases caused by the expanded polyglutamine-containing proteins. More than 20 transcription-related factors have been reported to interact with disease proteins, and the pathological interaction is known to repress gene expression. The whole shape of nuclear events evoked by disease proteins is now emerging with information on these transcription-related factors and with findings on the similarity between nuclear bodies and pathological inclusion bodies. This article reviews 'transcription theory', a rapidly growing hypothesis in polyglutamine diseases.

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“…For an ideal mouse model of SEB toxicosis and toxic shock, pathological reactions similar to those of monkeys or humans are a prerequisite. Actinomycin D (ACT-D) has been used to enhance the sensitivity of L929 cells to tumor necrosis factor in in vitro assays (26). It also has an additive effect with LPS and tumor necrosis factor in inducing lethal toxic shock in mice (6).…”

mentioning

confidence: 99%

Increased susceptibility to staphylococcal enterotoxin B intoxication in mice primed with actinomycin D

et al. 1994

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Mice (BALB/cJ, C3H/HeN, and C3HIHeJ) primed with actinomycin D became highly susceptible to lethal intoxication with staphylococcal enterotoxin B (SEB). The mice underwent toxicosis and toxic shock and died. Actinomycin D-primed C311/HeN and C3H/HeJ mice showed equal sensitivity to SEB, suggesting that bacterial lipopolysaccharide derived from gram-negative bacteria in the gut may not be an important cofactor in intoxication. In a time course study of the illness, prominent pathological changes characterized by blood congestion and thickening of alveolar septa were seen in the lung, while blood congestion, inflammation, epithelial cell flattening, and villous blunting were seen in the small intestine. In lymphoid tissues, such as the spleen, congestion, inflammation, and lymphoid cell depletion were the major reactions. The pathological features of the mice had many similarities to those of rhesus monkeys intoxicated with intravenous SEB. The actinomycin D-primed C3HI1eJ mice are thus an ideal mouse model for studying SEB toxicosis and toxic shock * Corresponding author.

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Induction of tumor necrosis factor synthesis in human monocytes treated by transcriptional inhibitors

Cited by 12 publications

References 6 publications

Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

Tumor necrosis factor-induced apoptosis during the poisoning of mice with hepatotoxins

Polyglutamine diseases: a transcription disorder?

Increased susceptibility to staphylococcal enterotoxin B intoxication in mice primed with actinomycin D

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