Expression of Fas Ligand in Activated T Cells Is Regulated by c-Myc

Brunner, Thomas; Kasibhatla, Shailaja; Pinkoski, Michael J.; Frutschi, Corina; Yoo, Nam Jin; Echeverri, Fernando; Mahboubi, Artin; Green, Douglas R.

doi:10.1074/jbc.275.13.9767

Cited by 79 publications

(78 citation statements)

References 46 publications

(42 reference statements)

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“…[12][13][14][15] Moreover, inhibition of activation-induced cell death (AICD) by TGFb correlates with downregulation of surface CD95L, a process mediated by c-myc in T-cell lines. 16,17 In B lymphocytes, downmodulation of c-myc expression correlates with induction of apoptosis in B-cell lines. [18][19][20] Anti-CD40 stimulation of B lymphocytes induces the surface expression of CD95 and makes them susceptible to cell death by this receptor.…”

Section: Introductionmentioning

confidence: 99%

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

2003

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C-myc gene is a member of the myc family of protooncogenes involved in proliferation, differentiation, and apoptosis. Overexpression of c-myc in fibroblasts causes apoptosis under low serum conditions in a process that requires the interaction of CD95 and CD95L on the surface. We have previously reported an in vivo conditional model to inactivate the c-myc gene in B lymphocytes. Here, we show that c-Myc-deficient primary B lymphocytes are resistant to different apoptotic stimuli. Nonactivated c-Myc-deficient B cells are resistant to spontaneous cell death. Upon activation, c-Myc-deficient B lymphocytes express normal surface levels of activation markers, and show resistance to staurosporine and CD95-induced cell death.

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Section: Introductionmentioning

confidence: 99%

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

2003

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“…However, neither CD95 nor TRAIL death receptors consistently activate NF-B (10,18), so c-Myc-induced sensitization to these death receptors must presumably involve other mechanisms. In T cells, there is evidence that c-Myc may directly up-regulate expression of the CD95 ligand (19). However, this mechanism does not explain how c-Myc induces global sensitivity to three different death receptors.…”

mentioning

confidence: 98%

c-Myc Augments the Apoptotic Activity of Cytosolic Death Receptor Signaling Proteins by Engaging the Mitochondrial Apoptotic Pathway

Klefström¹,

Verschuren

Evan

2002

Journal of Biological Chemistry

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“…Gln supplementation (12) and is dependent on Fas signaling (24,25), it is tempting to conjecture that Gln itself suppresses Fas-mediated apoptosis. To address this issue, we incubated HeLa cells in Gln-free medium overnight and administrated anti-Fas antibody for inducing apoptosis after supplementing Gln (0 and 4 mM, respectively).…”

Section: Glutamine Deprivation Sensitizes Hela Cells To Fas-mediated mentioning

confidence: 99%

Glutamine-dependent Antiapoptotic Interaction of Human Glutaminyl-tRNA Synthetase with Apoptosis Signal-regulating Kinase 1

Ko¹,

Kim²,

Kim³

et al. 2001

Journal of Biological Chemistry

181

123

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Glutamine has been known to be an apoptosis suppressor, since it blocks apoptosis induced by heat shock, irradiation, and c-Myc overexpression. Here, we demonstrated that HeLa cells were susceptible to Fas-mediated apoptosis under the condition of glutamine deprivation. Fas ligation activated apoptosis signalregulating kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK; also known as stress-activated protein kinase (SAPK)) in Gln-deprived cells but not in normal cells, suggesting that Gln might be involved in the activity control of ASK1 and JNK/SAPK. As one of the possible mechanisms for the suppressive effect of Gln on ASK1, we investigated the molecular interaction between human glutaminyl-tRNA synthetase (QRS) and ASK1 and found the Gln-dependent association of the two molecules. While their association was enhanced by the elevation of Gln concentration, they were dissociated by Fas ligation within 5 min. The association involved the catalytic domains of the two enzymes. The ASK1 activity was inhibited by the interaction with QRS as determined by in vitro kinase and transcription assays. Finally, we have shown that QRS inhibited the cell death induced by ASK1, and this antiapoptotic function of QRS was weakened by the deprivation of Gln. Thus, the antiapoptotic interaction of QRS with ASK1 is controlled positively by the cellular concentration of Gln and negatively by Fas ligation. The results of this work provide one possible explanation for the working mechanism of the antiapoptotic activity of Gln and suggest a novel function of mammalian ARSs.

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Expression of Fas Ligand in Activated T Cells Is Regulated by c-Myc

Cited by 79 publications

References 46 publications

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

c-Myc Augments the Apoptotic Activity of Cytosolic Death Receptor Signaling Proteins by Engaging the Mitochondrial Apoptotic Pathway

Glutamine-dependent Antiapoptotic Interaction of Human Glutaminyl-tRNA Synthetase with Apoptosis Signal-regulating Kinase 1

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