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Induction of apoptosis by a secreted lipocalin that is transcriptionally regulated by IL-3 deprivation

dc.contributor.authorDevireddy, Laxminarayana R.
dc.contributor.authorTeodoro, Jose G.
dc.contributor.authorRichard, Fabien A.
dc.contributor.authorGreen, Michael R.
dc.date2022-08-11T08:09:35.000
dc.date.accessioned2022-08-23T16:36:27Z
dc.date.available2022-08-23T16:36:27Z
dc.date.issued2001-08-04
dc.date.submitted2009-03-31
dc.identifier.citationScience. 2001 Aug 3;293(5531):829-34. <a href="http://dx.doi.org/10.1126/science.1061075">Link to article on publisher's site</a>
dc.identifier.issn0036-8075 (Print)
dc.identifier.doi10.1126/science.1061075
dc.identifier.pmid11486081
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38791
dc.description.abstractMany 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=11486081&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1126/science.1061075
dc.subjectAcute-Phase Proteins
dc.subjectAnimals
dc.subject*Apoptosis
dc.subjectAutocrine Communication
dc.subjectCarrier Proteins
dc.subjectCell Line
dc.subjectCells, Cultured
dc.subjectCulture Media, Conditioned
dc.subjectDexamethasone
dc.subject*Gene Expression Regulation
dc.subjectHumans
dc.subjectInsulin-Like Growth Factor I
dc.subjectInterleukin-3
dc.subjectInterleukins
dc.subjectLeukocytes
dc.subjectLipocalins
dc.subjectMice
dc.subjectOligonucleotide Array Sequence Analysis
dc.subjectOncogene Proteins
dc.subjectPhosphorylation
dc.subjectProto-Oncogene Proteins
dc.subjectProto-Oncogene Proteins c-bcl-2
dc.subjectReceptors, Cell Surface
dc.subjectRecombinant Fusion Proteins
dc.subjectTranscription, Genetic
dc.subjectTumor Cells, Cultured
dc.subjectbcl-Associated Death Protein
dc.subjectbcl-X Protein
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleInduction of apoptosis by a secreted lipocalin that is transcriptionally regulated by IL-3 deprivation
dc.typeJournal Article
dc.source.journaltitleScience (New York, N.Y.)
dc.source.volume293
dc.source.issue5531
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1636
dc.identifier.contextkey805457
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/1636
dc.contributor.departmentProgram in Gene Function and Expression
dc.contributor.departmentHoward Hughes Medical Institute, Program in Molecular Medicine
dc.source.pages829-34


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