Publication Date:
2001-08-04
Description:
Many hematopoietic cells undergo apoptosis when deprived of specific cytokines, and this process requires de novo RNA/protein synthesis. Using DNA microarrays to analyze interleukin-3 (IL-3)-dependent murine FL5.12 pro-B cells, we found that the gene undergoing maximal transcriptional induction after cytokine withdrawal is 24p3, which encodes a secreted lipocalin. Conditioned medium from IL-3-deprived FL5.12 cells contained 24p3 and induced apoptosis in naive FL5.12 cells even when IL-3 was present. 24p3 also induced apoptosis in a wide variety of leukocytes but not other cell types. Apoptotic sensitivity correlated with the presence of a putative 24p3 cell surface receptor. We conclude that IL-3 deprivation activates 24p3 transcription, leading to synthesis and secretion of 24p3, which induces apoptosis through an autocrine pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devireddy, L R -- Teodoro, J G -- Richard, F A -- Green, M R -- New York, N.Y. -- Science. 2001 Aug 3;293(5531):829-34.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Gene Function and Expression and Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11486081" target="_blank"〉PubMed〈/a〉
Keywords:
Acute-Phase Proteins/*genetics/*metabolism
;
Animals
;
*Apoptosis/drug effects
;
Autocrine Communication
;
Carrier Proteins/metabolism
;
Cell Line
;
Cells, Cultured
;
Culture Media, Conditioned
;
Dexamethasone/pharmacology
;
*Gene Expression Regulation
;
Humans
;
Insulin-Like Growth Factor I/pharmacology
;
Interleukin-3/*metabolism
;
Interleukins/metabolism
;
Leukocytes/cytology/*physiology
;
Lipocalins
;
Mice
;
Oligonucleotide Array Sequence Analysis
;
Oncogene Proteins/*genetics/*metabolism
;
Phosphorylation
;
Proto-Oncogene Proteins
;
Proto-Oncogene Proteins c-bcl-2/metabolism
;
Receptors, Cell Surface/metabolism
;
Recombinant Fusion Proteins/metabolism
;
Transcription, Genetic
;
Tumor Cells, Cultured
;
bcl-Associated Death Protein
;
bcl-X Protein
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
Permalink
