Evidence map›Paper›PMID 10430629›Full record

ArticleThe Journal of experimental medicine1999

Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein.

L Gabriele, J Phung, J Fukumoto, D Segal, I M Wang, P Giannakakou, N A Giese, K Ozato, H C Morse

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Relevance of Interferon Regulatory Factor-8 Expression in Myeloid-Tumor Interactions.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Review
  9. Regulation of myelopoiesis by the transcription factor IRF8.International journal of hematology · 2015
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Microglia development and function.Annual review of immunology · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

L GabrieleLaboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-0760, USA. lgabriele@atlas.niaid.nih.gov
J Phung
J Fukumoto
D Segal
I M Wang
P Giannakakou
N A Giese
K Ozato
H C Morse
National Institute of Allergy and Infectious Diseases · USHealth and Human Development (2HD) Research Network · CMNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice with a null mutation of the gene encoding interferon consensus sequence-binding protein (ICSBP) develop a disease with marked expansion of granulocytes and macrophages that frequently progresses to a fatal blast crisis, thus resembling human chronic myelogenous leukemia (CML). One important feature of CML is decreased responsiveness of myeloid cells to apoptotic stimuli. Here we show that myeloid cells from mice deficient in ICSBP exhibit reduced spontaneous apoptosis and a significant decrease in sensitivity to apoptosis induced by DNA damage. In contrast, apoptosis in thymocytes from ICSBP-deficient mice is unaffected. We also show that overexpression of ICSBP in the human U937 monocytic cell line enhances the rate of spontaneous apoptosis and the sensitivity to apoptosis induced by etoposide, lipopolysaccharide plus ATP, or rapamycin. Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases. Studies of proapoptotic genes showed that cells overexpressing ICSBP have enhanced expression of caspase-3 precursor protein. In addition, analyses of antiapoptotic genes showed that overexpression of ICSBP results in decreased expression of Bcl-X(L). These data suggest that ICSBP modulates survival of myeloid cells by regulating expression of apoptosis-related genes.

Indexed as

Amino Acid Chloromethyl KetonesAnimalsApoptosisbcl-X ProteinBone Marrow CellsCaspasesCells, CulturedConsensus SequenceCysteine Proteinase InhibitorsEtoposideGene Expression RegulationHematopoietic Stem CellsHumansInterferon Regulatory Factor-8Interferon Regulatory FactorsInterferonsAmino Acid Chloromethyl KetonesBCL2L1 protein, humanBcl2l1 protein, mousebcl-X Proteinbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCaspasesCysteine Proteinase InhibitorsEtoposideInterferon Regulatory Factor-8Interferon Regulatory FactorsInterferonsProto-Oncogene Proteins c-bcl-2Recombinant ProteinsRepressor Proteins

Identifiers

PMID10430629
PMCPMC2195590
OpenAlexW2115970169

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.