PI-3K/Akt and NF-?B/I?B? pathways are activated in Jurkat T cells in response to TRAIL treatment
- 10 September 2004
- journal article
- research article
- Published by Wiley in Journal of Cellular Physiology
- Vol. 202 (3), 900-911
- https://doi.org/10.1002/jcp.20202
Abstract
No abstract availableKeywords
This publication has 53 references indexed in Scilit:
- Constitutively active Akt1 protects HL60 leukemia cells from TRAIL-induced apoptosis through a mechanism involving NF-κB activation and cFLIPL up-regulationLeukemia, 2003
- Role of nuclear PKC ? in mediating caspase-3-upregulation in Jurkat T leukemic cells exposed to ionizing radiationJournal of Cellular Biochemistry, 2002
- On the TRAIL to apoptosisCytokine & Growth Factor Reviews, 2002
- IκB-α, the NF-κB Inhibitory Subunit, Interacts with ANT, the Mitochondrial ATP/ADP TranslocatorPublished by Elsevier BV ,2001
- Oxidative Stress Induces NF- B Nuclear Translocation Without Degradation of I BCirculation, 1999
- Apoptosis control by death and decoy receptorsCurrent Opinion in Cell Biology, 1999
- Involvement of regulatory and catalytic subunits of phosphoinositide 3-kinase in NF-κB activationProceedings of the National Academy of Sciences of the United States of America, 1999
- Regulation of Cell Death Protease Caspase-9 by PhosphorylationScience, 1998
- Death Receptor 5, a New Member of the TNFR Family, and DR4 Induce FADD-Dependent Apoptosis and Activate the NF-κB PathwayImmunity, 1997
- Tumor necrosis factor receptor superfamily members and their ligandsCurrent Opinion in Immunology, 1994