TNF-α activates at least two apoptotic signaling cascades

Fraisse, Carole Sidoti-de; Rincheval, Vincent; Risler, Yanick; Mignotte, Bernard; Vayssière, Jean-Luc

doi:10.1038/sj.onc.1202094

Cited by 132 publications

(20 citation statements)

References 55 publications

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“…4). Collectively, our data are contrary to the findings in mammalian cells that O 2 -W is not a messenger in the TNF pathway [8], but in agreement with those from HeLa cells that the generation of ROS is crucial for the TNF cytotoxicity [21].…”

Section: Discussioncontrasting

confidence: 57%

Tumour Necrosis Factor Induced an Early Release of Superoxide and a Late Mitochondrial Membrane Depolarization in L929 Cells

Kwok²,

Fung³

et al. 2001

Neurosignals

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Tumour necrosis factor α (TNF) cytotoxicity is mediated, at least in part, by oxidative stress. One of the post-receptor events shortly after the addition of TNF is the generation of the superoxide anion (O₂^–·). In the present study, we attempted to examine the role of O₂^–· in the regulation of mitochondrial membrane potential (ΔΨm) and the release of cytochrome c (cyto c) in L929 cells after stimulation with TNF. Challenge of cells with TNF (50 ng/ml) resulted in an early (30 min after the addition of TNF) increase in the production of O₂^–·. The use of mitochondrial electron transport chain inhibitors such as antimycin A and rotenone could, respectively, potentiate or suppress the TNF-mediated release of O₂^–· and cytotoxicity. TNF also induced a late (>3 h after the addition of TNF) depolarization in the ΔΨm. Reduction in the release of O₂^–· by rotenone (50 µM) or thenoyltrifluoroacetone (250 µM) suppressed both the TNF-mediated ΔΨm depolarization and cyto c release. However, increase in the production of O₂^–· by antimycin A (25 µM) only slightly enhanced the TNF effect in altering the ΔΨm and the release of cyto c. Treating cells with antimycin A alone could not induce a reduction in ΔΨm nor a release of cyto c. Taken together, our results indicate that TNF induced damage in mitochondria in L929 cells. Our data also show that an increase in the production of O₂^–· was important in the TNF cytotoxicity, but was not sufficient to mimic the action of TNF.

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Section: Discussioncontrasting

confidence: 57%

Tumour Necrosis Factor Induced an Early Release of Superoxide and a Late Mitochondrial Membrane Depolarization in L929 Cells

Kwok²,

Fung³

et al. 2001

Neurosignals

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“…Upon stimulation with pro-inflammatory cytokines, NF-κB induces the transcription of a number of anti-apoptotic genes (Barkett and Gilmore, 1999; Ghosh and Karin, 2002; Sidoti-de Fraisse et al, 1998). To investigate the biological significance of PPM1G in these processes, we analyzed its involvement in the apoptotic response regulated by NF-κB (Figure 5C).…”

Section: Resultsmentioning

confidence: 99%

Transcription Factors Mediate the Enzymatic Disassembly of Promoter-Bound 7SK snRNP to Locally Recruit P-TEFb for Transcription Elongation

et al. 2013

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SUMMARY The transition from transcription initiation into elongation is controlled by transcription factors, which recruit P-TEFb to promoters to phosphorylate RNA polymerase II. A fraction of P-TEFb is recruited as part of the inhibitory 7SK small nuclear ribonucleoprotein (snRNP), which inactivates the kinase and prevents elongation. It is unclear, however, how P-TEFb is captured from the promoter-bound 7SK snRNP to activate elongation. Here, we describe a novel mechanism by which transcription factors mediate the enzymatic release of P-TEFb from the 7SK snRNP at promoters to trigger activation in a gene-specific manner. We demonstrate that Tat recruits PPM1G/PP2Cγ to locally disassemble P-TEFb from the 7SK snRNP at the HIV promoter via dephosphorylation of the kinase T-loop. Similar to Tat, NF-κB recruits PPM1G in a stimulus-dependent manner to activate elongation at inflammatory-responsive genes. Recruitment of PPM1G to promoter-assembled 7SK snRNP provides a new paradigm for rapid gene activation through transcriptional pause release.

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“…Nitric oxide produced by iNOS is cytotoxic and each of these M1 markers is increased in brain and/or blood following brain injury or during inflammation (Dammann and Leviton, 1997; Hedtjarn et al, 2004; Helmy et al, 2011). In particular, increased IL-6 and TNFα is linked to a poor prognosis in infants suffering encephalopathy (Savman et al, 1998; Aly et al, 2006), these factors known to stimulate extrinsic pathways of cell death (Sidoti-de Fraisse et al, 1998). As such, these factors are assigned as M1-cytotoxic markers.…”

Section: Discussionmentioning

confidence: 99%

Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro

Chhor¹,

Charpentier²,

Lebon³

et al. 2013

Brain, Behavior, and Immunity

556

549

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TNF-α activates at least two apoptotic signaling cascades

Cited by 132 publications

References 55 publications

Tumour Necrosis Factor Induced an Early Release of Superoxide and a Late Mitochondrial Membrane Depolarization in L929 Cells

Tumour Necrosis Factor Induced an Early Release of Superoxide and a Late Mitochondrial Membrane Depolarization in L929 Cells

Transcription Factors Mediate the Enzymatic Disassembly of Promoter-Bound 7SK snRNP to Locally Recruit P-TEFb for Transcription Elongation

Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro

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