| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| M Vukmanovic-Stejic, B Vyas, P Gorak-Stolinska, A Noble, D M Kemen. Human Tc1 and Tc2/Tc0 CD8 T-cell clones display distinct cell surface and functional phenotypes. Blood. vol 95. issue 1. 2000-01-31. PMID:10607707. |
both tc1 and tc2/0 clones showed comparable cytotoxicity and produced similar levels of perforin and fas l. however, tc2 clones were much more resistant to activation-induced cell death and less susceptible to apoptosis by direct fas ligation. |
2000-01-31 |
2023-08-12 |
human |
| Y W He, M J Beva. High level expression of CD43 inhibits T cell receptor/CD3-mediated apoptosis. The Journal of experimental medicine. vol 190. issue 12. 2000-01-28. PMID:10601365. |
recent studies have demonstrated that engagement of tcr and fas induces naive cd4(+) t cells to undergo apoptosis, and the same treatment enhances the proliferation of memory cd4(+) t cells. |
2000-01-28 |
2023-08-12 |
Not clear |
| A Trifilieff, Y Futjitani, A J Coyle, C Bertran. Fas-induced death of a murine pulmonary epithelial cell line: modulation by inflammatory cytokines. Fundamental & clinical pharmacology. vol 13. issue 6. 2000-01-28. PMID:10626753. |
this increase in fas expression was associated with an increase in sensitivity to anti-fas-induced apoptosis of la-4 cells. |
2000-01-28 |
2023-08-12 |
Not clear |
| L Yel, S Aggarwal, S Gupt. Cartilage-hair hypoplasia syndrome: increased apoptosis of T lymphocytes is associated with altered expression of Fas (CD95), FasL (CD95L), IAP, Bax, and Bcl2. Journal of clinical immunology. vol 19. issue 6. 2000-01-28. PMID:10634217. |
cartilage-hair hypoplasia syndrome: increased apoptosis of t lymphocytes is associated with altered expression of fas (cd95), fasl (cd95l), iap, bax, and bcl2. |
2000-01-28 |
2023-08-12 |
Not clear |
| L Yel, S Aggarwal, S Gupt. Cartilage-hair hypoplasia syndrome: increased apoptosis of T lymphocytes is associated with altered expression of Fas (CD95), FasL (CD95L), IAP, Bax, and Bcl2. Journal of clinical immunology. vol 19. issue 6. 2000-01-28. PMID:10634217. |
increased apoptosis in chh was associated with increased expression of fas (cd95), cd95l, and bax and decreased expression of bcl-2 and inhibitor of apoptosis protein (iap) compared to the control. |
2000-01-28 |
2023-08-12 |
Not clear |
| D C Huang, M Hahne, M Schroeter, K Frei, A Fontana, A Villunger, K Newton, J Tschopp, A Strasse. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L). Proceedings of the National Academy of Sciences of the United States of America. vol 96. issue 26. 2000-01-27. PMID:10611305. |
activation of fas by fasl induces apoptosis by a mechanism that cannot be blocked by bcl-2 or bcl-x(l). |
2000-01-27 |
2023-08-12 |
mouse |
| D C Huang, M Hahne, M Schroeter, K Frei, A Fontana, A Villunger, K Newton, J Tschopp, A Strasse. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L). Proceedings of the National Academy of Sciences of the United States of America. vol 96. issue 26. 2000-01-27. PMID:10611305. |
fas activation triggers apoptosis in many cell types. |
2000-01-27 |
2023-08-12 |
mouse |
| D C Huang, M Hahne, M Schroeter, K Frei, A Fontana, A Villunger, K Newton, J Tschopp, A Strasse. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L). Proceedings of the National Academy of Sciences of the United States of America. vol 96. issue 26. 2000-01-27. PMID:10611305. |
comparison between physiological ligand and anti-fas antibodies revealed that only extensive fas aggregation, by membrane bound fasl or aggregated soluble fasl consistently triggered apoptosis, whereas antibodies could act as death agonists or antagonists. |
2000-01-27 |
2023-08-12 |
mouse |
| D C Huang, M Hahne, M Schroeter, K Frei, A Fontana, A Villunger, K Newton, J Tschopp, A Strasse. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L). Proceedings of the National Academy of Sciences of the United States of America. vol 96. issue 26. 2000-01-27. PMID:10611305. |
studies on fas signaling in cell lines and primary cells from transgenic mice revealed that fadd/mort1 and caspase-8 were required for apoptosis. |
2000-01-27 |
2023-08-12 |
mouse |
| D C Huang, M Hahne, M Schroeter, K Frei, A Fontana, A Villunger, K Newton, J Tschopp, A Strasse. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L). Proceedings of the National Academy of Sciences of the United States of America. vol 96. issue 26. 2000-01-27. PMID:10611305. |
in contrast, bcl-2 or bcl-x(l) did not block fasl-induced apoptosis in lymphocytes or hepatocytes, demonstrating that signaling for cell death induced by fas and the pathways to apoptosis regulated by the bcl-2 family are distinct. |
2000-01-27 |
2023-08-12 |
mouse |
| J Albanese, N Dainia. Ionizing radiation alters Fas antigen ligand at the cell surface and on exfoliated plasma membrane-derived vesicles: implications for apoptosis and intercellular signaling. Radiation research. vol 153. issue 1. 2000-01-27. PMID:10630977. |
ionizing radiation alters fas antigen ligand at the cell surface and on exfoliated plasma membrane-derived vesicles: implications for apoptosis and intercellular signaling. |
2000-01-27 |
2023-08-12 |
Not clear |
| J Albanese, N Dainia. Ionizing radiation alters Fas antigen ligand at the cell surface and on exfoliated plasma membrane-derived vesicles: implications for apoptosis and intercellular signaling. Radiation research. vol 153. issue 1. 2000-01-27. PMID:10630977. |
when assayed for bioactivity, vesicles from unexposed cells induced the greatest level of apoptosis in tnfrsf6 (formerly known as fas) receptor-bearing jurkat cells (cell surviving fraction of 43.7 +/- 6.1; p < 0.05), followed by vesicles collected from cells treated with 4 gy (79.6 +/- 2.6%; p < 0.05). |
2000-01-27 |
2023-08-12 |
Not clear |
| T Kiba, S Saito, K Numata, H Sekihar. Fas (APO-1/CD95) mRNA is down-regulated in liver regeneration after hepatectomy in rats. Journal of gastroenterology. vol 35. issue 1. 2000-01-27. PMID:10632538. |
the interaction of fas (apo-1/cd95) and the fas ligand system induces apoptosis. |
2000-01-27 |
2023-08-12 |
rat |
| J Wang, A A Lobito, F Shen, F Hornung, A Winoto, M J Lenard. Inhibition of Fas-mediated apoptosis by the B cell antigen receptor through c-FLIP. European journal of immunology. vol 30. issue 1. 2000-01-24. PMID:10602037. |
cross-linking of the b cell antigen receptor (bcr) induces resistance to fas (apo-1 / cd95)-dependent apoptosis and thereby regulates one mechanism of b cell selection during antigen stimulation. |
2000-01-24 |
2023-08-12 |
Not clear |
| L Guéry, F Batteux, N Bessis, M Breban, M C Boissier, C Fournier, G Chiocchi. Expression of Fas ligand improves the effect of IL-4 in collagen-induced arthritis. European journal of immunology. vol 30. issue 1. 2000-01-24. PMID:10602054. |
these findings suggest that the mechanism underlying the beneficial effect of il-4 delivered by cells expressing fasl involves the combination of the anti-inflammatory properties of il-4 and the apoptosis of fas(+) mac1(+) granulocytes participating in the pathogenic process. |
2000-01-24 |
2023-08-12 |
mouse |
| H C Hsu, J D Mountz, T Zho. Regulation of Fas-mediated apoptosis in CD2-fas transgenic mice. International reviews of immunology. vol 18. issue 4. 2000-01-24. PMID:10626246. |
correction of fas in fas-mutant mice restored apoptosis function and ameliorated autoimmune symptoms, whereas a long-term enhancement of fas expression in fas-normal mice resulted in an increased acute-phase response and renal amyloidosis in aged transgenic mice. |
2000-01-24 |
2023-08-12 |
mouse |
| J Wang, T Watanab. Expression and function of Fas during differentiation and activation of B cells. International reviews of immunology. vol 18. issue 4. 2000-01-24. PMID:10626249. |
fas (apo-1, cd95) cell surface antigen belongs to the tumor necrosis factor receptor family and mediates apoptosis of a variety of cell types, including lymphocytes, after ligation with fas ligand (fasl). |
2000-01-24 |
2023-08-12 |
Not clear |
| R Wang, A Zagariya, E Ang, O Ibarra-Sunga, B D Uha. Fas-induced apoptosis of alveolar epithelial cells requires ANG II generation and receptor interaction. The American journal of physiology. vol 277. issue 6. 2000-01-20. PMID:10600897. |
these findings led us to hypothesize that the synthesis and binding of ang ii to its receptor might be involved in the induction of aec apoptosis by fas. |
2000-01-20 |
2023-08-12 |
human |
| R Wang, A Zagariya, E Ang, O Ibarra-Sunga, B D Uha. Fas-induced apoptosis of alveolar epithelial cells requires ANG II generation and receptor interaction. The American journal of physiology. vol 277. issue 6. 2000-01-20. PMID:10600897. |
apoptosis was induced in the aec-derived human lung carcinoma cell line a549 or in primary aecs isolated from adult rats with receptor-activating anti-fas antibodies or purified recombinant fas ligand, respectively. |
2000-01-20 |
2023-08-12 |
human |
| R Wang, A Zagariya, E Ang, O Ibarra-Sunga, B D Uha. Fas-induced apoptosis of alveolar epithelial cells requires ANG II generation and receptor interaction. The American journal of physiology. vol 277. issue 6. 2000-01-20. PMID:10600897. |
apoptosis in response to either fas activator was inhibited in a dose-dependent manner by the nonthiol ace inhibitor lisinopril or the nonselective ang ii receptor antagonist saralasin, with maximal inhibitions of 82 and 93% at doses of 0.5 and 5 microg/ml, respectively. |
2000-01-20 |
2023-08-12 |
human |