Evidence map›Paper›PMID 12944488›Full record

ArticleMolecular and cellular biology2003

Molecular mechanisms associated with the regulation of apoptosis by the two alternatively spliced products of c-Myb.

Atul Kumar, Stacey J Baker, Clement M Lee, E Premkumar Reddy

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011
    Review
  6. Article
  7. Article
  8. p89c-Myb is not required for fetal or adult hematopoiesis.Genesis (New York, N.Y. : 2000) · 2010
    Article
  9. Article
  10. Article
  11. Article
  12. The gene encoding the splicing factor SF2/ASF is a proto-oncogene.Nature structural & molecular biology · 2007
    Article
  13. Article
  14. Article
  15. A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Atul KumarFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N. Broad Street, Philadelphia, PA 19140, USA.
Stacey J Baker
Clement M Lee
E Premkumar Reddy
Montefiore Medical Center · US

Funding

SHARED RESOURCES FOR CANCER RESEARCHR24CA088261 · NCI · TEMPLE UNIVERSITY · PI REDDY, E PREMKUMAR · 2001 to 2005
$1.3M
MYB GENE FAMILY AND BREAST CANCERR01CA079086 · NCI · TEMPLE UNIVERSITY · PI REDDY, E PREMKUMAR · 1999 to 2003
$1.2M
NCI NIH HHS CA 79086NCI NIH HHS R01 CA079086NCI NIH HHS R24 CA088261NCI NIH HHS R24 CA 88261
6 · The paper itself

Abstract

The c-myb proto-oncogene encodes two alternatively spliced mRNAs, which in turn code for proteins of 75 kDa and 89 kDa. It is at present unclear whether the two isoforms of c-Myb perform identical functions or whether they mediate different biological effects. To assess their role in apoptotic death of hematopoietic cells, we expressed the two isoforms of c-Myb in the murine myeloid cell lines 32Dcl3 and FDCP1. Our results show that while ectopic overexpression of p75 c-Myb results in the acceleration of cell death, similar overexpression of p89 c-Myb results in the protection of cells from apoptotic death. An analysis of gene expression changes with mouse cDNA expression arrays revealed that while p75 c-Myb blocked the expression of glutathione S-transferase micro mRNA, p89 c-Myb greatly enhanced the expression of this gene. These results were further confirmed by Northern blot analysis. Ectopic overexpression of the glutathione S-transferase micro gene in 32Dcl3 cells resulted in protection of cells from interleukin-3 withdrawal-induced cell death similar to that seen with the ectopic overexpression of p89 c-Myb. These results suggest that the two isoforms of c-Myb differentially regulate apoptotic death of myeloid cells through differential regulation of glutathione S-transferase micro gene expression.

Indexed as

Alternative SplicingAnimalsApoptosisBone Marrow CellsCaspasesCells, CulturedCytochrome c GroupEnzyme ActivationGene Expression RegulationGlutathione TransferaseInterleukin-3MiceMutationMyeloid CellsOligonucleotides, AntisenseProtein IsoformsCaspasesCytochrome c GroupGlutathione TransferaseInterleukin-3Oligonucleotides, AntisenseProtein IsoformsProto-Oncogene Proteins c-myb

Identifiers

PMID12944488
PMCPMC193713
OpenAlexW2129143765

What OpenQuestion holds

Textmetadata
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.