| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| P G Ekert, J Silke, D L Vau. Inhibition of apoptosis and clonogenic survival of cells expressing crmA variants: optimal caspase substrates are not necessarily optimal inhibitors. The EMBO journal. vol 18. issue 2. 1999-03-15. PMID:9889190. |
wild-type crma inhibits caspases 1 and 8 and thereby protects cells from apoptosis triggered by ligation of cd95 or tumour necrosis factor (tnf) receptors, but it does not protect against death mediated by other caspases. |
1999-03-15 |
2023-08-12 |
Not clear |
| S Dan, M Naito, H Seimiya, A Kizaki, T Mashima, T Tsuru. Activation of c-Abl tyrosine kinase requires caspase activation and is not involved in JNK/SAPK activation during apoptosis of human monocytic leukemia U937 cells. Oncogene. vol 18. issue 6. 1999-03-03. PMID:10022809. |
we herein investigated the kinase activities of c-abl and jnk1/sapk during apoptosis elicited by genotoxic anticancer drugs and tumor necrosis factor (tnf) in u937 cells and their apoptosis-resistant variant uk711 cells. |
1999-03-03 |
2023-08-12 |
human |
| P S Koh, G C Hughes, G R Faulkner, W W Keeble, G C Bagb. The Fanconi anemia group C gene product modulates apoptotic responses to tumor necrosis factor-alpha and Fas ligand but does not suppress expression of receptors of the tumor necrosis factor receptor superfamily. Experimental hematology. vol 27. issue 1. 1999-02-25. PMID:9923438. |
because the ifn-gamma hypersensitivity of cells lacking the fac protein is mediated, in part, through priming of the fas pathway, and because several other members of this family are capable of inducing apoptosis either alone or in concert with each other, we tested the hypothesis that ifn-gamma induces increased expression of members of the tnf receptor (tnfr) superfamily in cells nullizygous for the fac gene. |
1999-02-25 |
2023-08-12 |
mouse |
| N H James, J H Gill, R Brindle, N J Woodyatt, N Macdonald, M Rolfe, S C Hasmall, J D Tugwood, P R Holden, R A Robert. Peroxisome proliferator-activated receptor (PPAR) alpha-regulated growth responses and their importance to hepatocarcinogenesis. Toxicology letters. vol 102-103. 1999-02-25. PMID:10022238. |
more recently, we have demonstrated that pps can suppress apoptosis induced by more diverse stimuli such as dna damage or ligation of fas, a receptor related to the tumour necrosis factor alpha (tnf alpha) family of cell surface receptors. |
1999-02-25 |
2023-08-12 |
human |
| M Perez, B Haschke, N J Donat. Differential expression and translocation of protein tyrosine phosphatase 1B-related proteins in ME-180 tumor cells expressing apoptotic sensitivity and resistance to tumor necrosis factor: potential interaction with epidermal growth factor receptor. Oncogene. vol 18. issue 4. 1999-02-23. PMID:10023672. |
tumor necrosis factor (tnf)-induced apoptosis can be inhibited by overexpression of specific tyrosine kinases or activation of tyrosine kinase cascades, suggesting potential antagonism between apoptotic and tyrosine kinase signaling processes. |
1999-02-23 |
2023-08-12 |
Not clear |
| M Perez, B Haschke, N J Donat. Differential expression and translocation of protein tyrosine phosphatase 1B-related proteins in ME-180 tumor cells expressing apoptotic sensitivity and resistance to tumor necrosis factor: potential interaction with epidermal growth factor receptor. Oncogene. vol 18. issue 4. 1999-02-23. PMID:10023672. |
prior to the onset of apoptosis, tnf caused a significant reduction in the level of egfr tyrosine phosphorylation in sen cells but mediated only limited suppression of egfr tyrosine phosphorylation in apoptotically resistant res cells. |
1999-02-23 |
2023-08-12 |
Not clear |
| R W Johnstone, E Cretney, M J Smyt. P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death. Blood. vol 93. issue 3. 1999-02-18. PMID:9920858. |
herein we show that cells induced to express p-glycoprotein either by drug selection or by retroviral gene transduction with mdr1 cdna are resistant to cell death induced by a wide range of death stimuli, such as fasl, tumor necrosis factor (tnf), and ultraviolet (uv) irradiation, that activate the caspase apoptotic cascade.however, p-glycoprotein-expressing cells were not resistant to caspase-independent cell death mediated by pore-forming proteins and granzyme b.mdr p-glycoprotein-expressing cells were made sensitive to caspase-dependent apoptosis by the addition of anti-p-glycoprotein antibodies or verapamil, a pharmacological inhibitor of p-glycoprotein function. |
1999-02-18 |
2023-08-12 |
Not clear |
| D W Seol, T R Billia. A caspase-9 variant missing the catalytic site is an endogenous inhibitor of apoptosis. The Journal of biological chemistry. vol 274. issue 4. 1999-02-16. PMID:9890966. |
moreover, caspase-9s inhibited apoptosis induced by tumor necrosis factor(tnf)-alpha, tnf factor-related apoptosis-inducing ligand (trail), bax, or fas-associated death domain-containing protein (fadd) as well as the combination of apaf-1 and caspase-9. |
1999-02-16 |
2023-08-12 |
human |
| N S Chang, J Mattison, H Cao, N Pratt, Y Zhao, C Le. Cloning and characterization of a novel transforming growth factor-beta1-induced TIAF1 protein that inhibits tumor necrosis factor cytotoxicity. Biochemical and biophysical research communications. vol 253. issue 3. 1999-02-09. PMID:9918798. |
l929 stable transfectants expressing tiaf1 do not have significant changes in the expression of tnf receptors and effector or regulatory proteins in apoptosis, which may account for the acquired tnf resistance in these cells. |
1999-02-09 |
2023-08-12 |
Not clear |
| Y Jiang, J D Woronicz, W Liu, D V Goedde. Prevention of constitutive TNF receptor 1 signaling by silencer of death domains. Science (New York, N.Y.). vol 283. issue 5401. 1999-02-08. PMID:9915703. |
tumor necrosis factor receptor type 1 (tnf-r1) contains a cytoplasmic death domain that is required for the signaling of tnf activities such as apoptosis and nuclear factor kappa b (nf-kappab) activation. |
1999-02-08 |
2023-08-12 |
Not clear |
| L A Gravestein, J Bors. Tumor necrosis factor receptor family members in the immune system. Seminars in immunology. vol 10. issue 6. 1999-02-05. PMID:9826575. |
the tumor necrosis factor (tnf) receptor family contains death receptors, which have a cytoplasmic death domain and can induce apoptosis, as well as receptors with no apparent homology in the cytoplasmic tail. |
1999-02-05 |
2023-08-12 |
mouse |
| M P Scheid, I N Foltz, P R Young, J W Schrader, V Duroni. Ceramide and cyclic adenosine monophosphate (cAMP) induce cAMP response element binding protein phosphorylation via distinct signaling pathways while having opposite effects on myeloid cell survival. Blood. vol 93. issue 1. 1999-02-04. PMID:9864164. |
a selective p38 mapk inhibitor, sb203580, blocked tnf-- or ceramide-induced creb phosphorylation, but had no effect on the induction of apoptosis mediated by these agents. |
1999-02-04 |
2023-08-12 |
human |
| M P Scheid, I N Foltz, P R Young, J W Schrader, V Duroni. Ceramide and cyclic adenosine monophosphate (cAMP) induce cAMP response element binding protein phosphorylation via distinct signaling pathways while having opposite effects on myeloid cell survival. Blood. vol 93. issue 1. 1999-02-04. PMID:9864164. |
in addition, because sb203580 had no effect of tnf- or ceramide-induced apoptosis, our results strongly argue against a role for p38 mapk in the induction of tnf-- or ceramide-induced apoptosis. |
1999-02-04 |
2023-08-12 |
human |
| M Bitzer, F Prinz, M Bauer, M Spiegel, W J Neubert, M Gregor, K Schulze-Osthoff, U Laue. Sendai virus infection induces apoptosis through activation of caspase-8 (FLICE) and caspase-3 (CPP32). Journal of virology. vol 73. issue 1. 1999-01-28. PMID:9847376. |
so far, activation of flice/caspase-8 has been described in apoptosis triggered by death receptors, including cd95 and tumor necrosis factor (tnf)-r1. |
1999-01-28 |
2023-08-12 |
Not clear |
| M Bitzer, F Prinz, M Bauer, M Spiegel, W J Neubert, M Gregor, K Schulze-Osthoff, U Laue. Sendai virus infection induces apoptosis through activation of caspase-8 (FLICE) and caspase-3 (CPP32). Journal of virology. vol 73. issue 1. 1999-01-28. PMID:9847376. |
in contrast, we could show that sv-induced apoptosis did not require tnf or cd95 ligand. |
1999-01-28 |
2023-08-12 |
Not clear |
| P Ribeiro, N Renard, K Warzocha, C Charlot, L Jeandenant, E Callet-Bauchu, B Coiffier, G Salle. CD40 regulation of death domains containing receptors and their ligands on lymphoma B cells. British journal of haematology. vol 103. issue 3. 1999-01-27. PMID:9858217. |
within the tumour necrosis factor (tnf) family the induction of apoptosis is restricted to some ligand-receptors pairs, including tnf-tnf receptor type i (tnfri/p55), fasl-fas, tnf-related apoptosis-inducing ligand (trail) and its death-receptors (dr)-4 and -5. |
1999-01-27 |
2023-08-12 |
human |
| S Lemaire, G Lizard, S Monier, C Miguet, S Gueldry, F Volot, P Gambert, D Née. Different patterns of IL-1beta secretion, adhesion molecule expression and apoptosis induction in human endothelial cells treated with 7alpha-, 7beta-hydroxycholesterol, or 7-ketocholesterol. FEBS letters. vol 440. issue 3. 1999-01-25. PMID:9872417. |
here, we asked whether all oxysterols oxidized at c7 were able to trigger apoptosis, to stimulate interleukin (il)-ibeta and/or tumor necrosis factor (tnf)-alpha secretion, and to enhance adhesion molecule expression (intercellular adhesion molecule-1 (icam-1), vascular cell adhesion molecule-1 (vcam-1), and e-selectin) on human umbilical venous endothelial cells (huvecs). |
1999-01-25 |
2023-08-12 |
human |
| D S Gary, A J Bruce-Keller, M S Kindy, M P Mattso. Ischemic and excitotoxic brain injury is enhanced in mice lacking the p55 tumor necrosis factor receptor. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. vol 18. issue 12. 1999-01-08. PMID:9850139. |
when taken together with recent data showing that tnf can prevent apoptosis of cultured neurons exposed to oxidative and metabolic insults, our findings suggest that tnf plays a neuroprotective role after acute brain insults. |
1999-01-08 |
2023-08-12 |
mouse |
| W X Zong, J Bash, C Gélina. Rel blocks both anti-Fas- and TNF alpha-induced apoptosis and an intact Rel transactivation domain is essential for this effect. Cell death and differentiation. vol 5. issue 11. 1998-12-30. PMID:9846183. |
rel blocks both anti-fas- and tnf alpha-induced apoptosis and an intact rel transactivation domain is essential for this effect. |
1998-12-30 |
2023-08-12 |
Not clear |
| W X Zong, J Bash, C Gélina. Rel blocks both anti-Fas- and TNF alpha-induced apoptosis and an intact Rel transactivation domain is essential for this effect. Cell death and differentiation. vol 5. issue 11. 1998-12-30. PMID:9846183. |
the v-rel oncoprotein must be continuously expressed to prevent the apoptosis of transformed lymphoid cells, and also inhibits tnf alpha-induced cell death. |
1998-12-30 |
2023-08-12 |
Not clear |