Document Detail

A1 is a growth-permissive antiapoptotic factor mediating postactivation survival in T cells.
MedLine Citation:
PMID:  12406903     Owner:  NLM     Status:  MEDLINE    
The regulation of cell death in activated naive T cells is not well understood. We examined the expression of A1, an antiapoptotic member of the Bcl-2 family, following activation of naive mouse splenocytes. A1 gene expression was strongly but transiently induced during the first day of activation, with a peak at 2 to 6 hours, whereas Bcl-2 mRNA was simultaneously transiently down-regulated. Transgenic (Tg) overexpression of A1-a in T cells via the lck distal promoter resulted in decreased apoptosis following activation either with concanavalin A or with antibodies to CD3 and CD28 and led to a doubling of T-cell yield by 5 days. Tg A1-a also partially protected thymocytes from several proapoptotic stimuli but did not protect T-cell blasts from cell death induced by reactivation via the T-cell receptor. Tg Bcl-2 and Tg A1-a showed a similar ability to reduce apoptosis in both resting and activated T cells. However, in activated splenocyte cultures, the increase in 5-day T-cell yield observed with Tg Bcl-2 was only half that produced by Tg A1-a. This difference could be attributed at least in part to the fact that A1, unlike Bcl-2, did not inhibit S-phase entry of activated cells. The A1 protein may represent an adaptation of the Bcl-2 gene family to the need for survival regulation in the context of a proliferative stimulus.
Juana Gonzalez; Amos Orlofsky; Michael B Prystowsky
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2002-10-24
Journal Detail:
Title:  Blood     Volume:  101     ISSN:  0006-4971     ISO Abbreviation:  Blood     Publication Date:  2003 Apr 
Date Detail:
Created Date:  2003-03-18     Completed Date:  2003-05-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2679-85     Citation Subset:  AIM; IM    
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
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MeSH Terms
Cell Division
Cell Survival
DNA-Binding Proteins / biosynthesis,  genetics,  physiology*
Gene Expression Regulation
Lymphocyte Activation*
Mice, Transgenic
Proto-Oncogene Proteins c-bcl-2 / genetics,  physiology
RNA, Messenger / biosynthesis
Replication Protein C
Spleen / cytology
T-Lymphocytes / cytology*,  metabolism
Thymus Gland / cytology
Grant Support
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/RNA, Messenger; 0/Replication Protein C

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