Journal
IMMUNITY
Volume 18, Issue 3, Pages 331-342Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(03)00053-0
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Funding
- NCI NIH HHS [2 P30 CA 46934-09, R01 CA077314, R01 CA077314-05, R01 CA077314-06, CA77314] Funding Source: Medline
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We have explored the interactions between the NFkappaB and Cdk-Rb-E2F pathways in controlling T cell fate following antigen stimulation. The inhibition of NFkappaB in antigen-stimulated T cells results in apoptosis but does not inhibit E2F activation and S phase entry. IkappaB-induced apoptosis coincides with the superinduction of p73 expression and activity. G1 Cdk activity is required for IkappaB-induced apoptosis and the induction of p73. Importantly, p73 deficiency rescues activated T cells from the apoptosis resulting from the inhibition of NFkappaB. Thus, Cdk2 activation sends signals for both cell cycle progression and apoptosis, the latter of which must be blocked by NFkappaB to allow for proliferation.
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