The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kiefer, J
Right arrow Articles by McConkey, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kiefer, J
Right arrow Articles by McConkey, D.

The Journal of Immunology, Vol 155, Issue 10 4525-4528, Copyright © 1995 by American Association of Immunologists

CUTTING EDGE

Functional glucocorticoid receptor expression is required for cAMP- mediated apoptosis in a human leukemic T cell line

J Kiefer, S Okret, M Jondal and DJ McConkey
Department of Cell Biology, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

The involvement of the glucocorticoid receptor (GR) in cAMP-induced apoptosis in a GR-deficient derivative of the CEM.C7 human T-ALL line was investigated. Incubation of the parental CEM.C7 cells with agents that elevate cAMP levels (dibutyryl cAMP and forskolin) resulted in DNA fragmentation characteristic of apoptotic cell death, whereas the GR- deficient ICR.27 cells were insensitive to the cytolytic effects of cAMP. Reconstitution of GR expression by transfection not only restored glucocorticoid sensitivity to the ICR.27 cells, but also promoted sensitivity to induction of apoptosis by cAMP. Thus, cAMP-induced apoptosis in T cells appears to occur via ligand-independent stimulation of at least some aspects of glucocorticoid receptor function.


This article has been cited by other articles:


Home page
 Clin. Cancer Res.Home page
J. A. Meyers, J. Taverna, J. Chaves, A. Makkinje, and A. Lerner
Phosphodiesterase 4 Inhibitors Augment Levels of Glucocorticoid Receptor in B Cell Chronic Lymphocytic Leukemia but Not in Normal Circulating Hematopoietic Cells
Clin. Cancer Res., August 15, 2007; 13(16): 4920 - 4927.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
R. Ogawa, M. B. Streiff, A. Bugayenko, and G. J. Kato
Inhibition of PDE4 phosphodiesterase activity induces growth suppression, apoptosis, glucocorticoid sensitivity, p53, and p21WAF1/CIP1 proteins in human acute lymphoblastic leukemia cells
Blood, May 1, 2002; 99(9): 3390 - 3397.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
M. P. Scheid, I. N. Foltz, P. R. Young, J. W. Schrader, and V. Duronio
Ceramide and Cyclic Adenosine Monophosphate (cAMP) Induce cAMP Response Element Binding Protein Phosphorylation via Distinct Signaling Pathways While Having Opposite Effects on Myeloid Cell Survival
Blood, January 1, 1999; 93(1): 217 - 225.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
D. H. Kim and A. Lerner
Type 4 Cyclic Adenosine Monophosphate Phosphodiesterase as a Therapeutic Target in Chronic Lymphocytic Leukemia
Blood, October 1, 1998; 92(7): 2484 - 2494.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. C. Martin, I. Dransfield, C. Haslett, and A. G. Rossi
Cyclic AMP Regulation of Neutrophil Apoptosis Occurs via a Novel Protein Kinase A-independent Signaling Pathway
J. Biol. Chem., November 21, 2001; 276(48): 45041 - 45050.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.