Regulation of FAS Ligand Expression during Activation-Induced Cell Death in T Cells by p38 Mitogen-Activated Protein Kinase and C-Jun Nh2-Terminal Kinase
Open Access
- 20 March 2000
- journal article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 191 (6) , 1017-1030
- https://doi.org/10.1084/jem.191.6.1017
Abstract
Activation-induced cell death (AICD) is a mechanism of peripheral T cell tolerance that depends upon an interaction between Fas and Fas ligand (FasL). AlthoughKeywords
This publication has 57 references indexed in Scilit:
- Apoptosis by Death FactorCell, 1997
- Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-κB Activation Prevents Cell DeathCell, 1996
- FLICE, A Novel FADD-Homologous ICE/CED-3–like Protease, Is Recruited to the CD95 (Fas/APO-1) Death-Inducing Signaling ComplexCell, 1996
- ICE Family Proteases: Mediators of All Apoptotic Cell Death?Immunity, 1996
- CPP32/Apopain Is a Key Interleukin 1β Converting Enzyme-like Protease Involved in Fas-mediated ApoptosisJournal of Biological Chemistry, 1996
- Persistent Activation of c-Jun N-terminal Kinase 1 (JNK1) in γ Radiation-induced ApoptosisJournal of Biological Chemistry, 1996
- Involvement of multiple proteases during Fas-mediated apoptosis in T lymphocytesFEBS Letters, 1995
- Fas(CD95)/FasL interactions required for programmed cell death after T-cell activationNature, 1995
- Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomasNature, 1995
- Fas and Fas ligand: lpr and gld mutationsImmunology Today, 1995