Bax Deficiency Partially Corrects Interleukin-7 Receptor α Deficiency
- 30 November 2002
- journal article
- Published by Elsevier BV in Immunity
- Vol. 17 (5), 561-573
- https://doi.org/10.1016/s1074-7613(02)00450-8
Abstract
No abstract availableKeywords
This publication has 45 references indexed in Scilit:
- FKHR-L1 can act as a critical effector of cell death induced by cytokine withdrawalThe Journal of cell biology, 2002
- Cellular damage signals promote sequential changes at the N-terminus and BH-1 domain of the pro-apoptotic protein BakOncogene, 2001
- Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and DeathScience, 2001
- Interleukin-3 Withdrawal Induces an Early Increase in Mitochondrial Membrane Potential Unrelated to the Bcl-2 FamilyPublished by Elsevier BV ,2001
- 14-3-3 Proteins and Survival Kinases Cooperate to Inactivate BAD by BH3 Domain PhosphorylationMolecular Cell, 2000
- Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase AktScience, 1997
- Bcl-2 Rescues T Lymphopoiesis, but Not B or NK Cell Development, in Common γ Chain–Deficient MiceImmunity, 1997
- Bcl-2 Can Rescue T Lymphocyte Development in Interleukin-7 Receptor–Deficient Mice but Not in Mutant rag-1−/− MiceCell, 1997
- Interleukin‐7 induces the association of phosphatidylinositol 3‐kinase with the α chain of the interleukin‐7 receptorEuropean Journal of Immunology, 1994
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993