Evidence map›Paper›PMID 15967790›Full record

ArticleThe Journal of biological chemistry2005

MAPK-mediated phosphorylation of GATA-1 promotes Bcl-XL expression and cell survival.

Yung-Luen Yu, Yun-Jung Chiang, Yu-Chun Chen, Michael Papetti, Chiun-Gung Juo, Arthur I Skoultchi, Jeffrey J Y Yen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Mechanism of inhibition of Shiga-toxigenicCell death discovery · 2018
    Article
  5. Article
  6. Article
  7. Article
  8. Transcriptional mechanisms underlying hemoglobin synthesis.Cold Spring Harbor perspectives in medicine · 2013
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

7 authors at 2 institutions in 2 countries.

Yung-Luen YuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Yun-Jung Chiang
Yu-Chun Chen
Michael Papetti
Chiun-Gung Juo
Arthur I Skoultchi
Jeffrey J Y Yen
Institute of Biomedical Sciences, Academia Sinica · TWAlbert Einstein College of Medicine · US

Funding

CBT and Modafinil for Cocaine AddictionR01DA016368 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MALCOLM, ROBERT JAMES · 2003 to 2009
$2.3M
Control of Erythroid Cell Division and DifferentiationR01HL078381 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI SKOULTCHI, ARTHUR I · 2004 to 2008
$2.1M
Role of GATA-1 in p21 Gene TranscriptionF32HL077242 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI PAPETTI, MICHAEL J · 2004 to 2006
$149k
NHLBI NIH HHS HL077242-01NHLBI NIH HHS HL78381-30NIDA NIH HHS R01 DA016368
6 · The paper itself

Abstract

In the interleukin 3-dependent hematopoietic cell line Ba/F3, inhibition of mitogen-activated protein kinase, a member of the MAPK/c-Jun N-terminal kinase/stress-activated protein kinase kinase family that plays an important role in cell growth and death control, rapidly leads to severe apoptosis. However, most of the antiapoptotic substrates of MAPK remain to be identified. Here we report that, upon interleukin-3 stimulation of Ba/F3 cells, the transcription factor GATA-1 is strongly phosphorylated at residue serine 26 by a MAPK-dependent pathway. Phosphorylation of GATA-1 increases GATA-1-mediated transcription of the E4bp4 survival gene without significantly changing the DNA-binding affinity of GATA-1. Further characterization of GATA-1 phosphorylation site mutants revealed that the antiapoptotic function of GATA-1 is strongly dependent upon its phosphorylation at the Ser-26 position and is probably mediated through its up-regulation of Bcl-X(L) expression. Taken together, our data demonstrate that MAPK-dependent GATA-1 phosphorylation is important for its transactivation of the E4bp4 gene, Bcl-X(L) expression and cell survival. Therefore, GATA-1 may represent a novel MAPK substrate that plays an essential role in a cytokine-mediated antiapoptotic response.

Indexed as

AnimalsBasic-Leucine Zipper Transcription Factorsbcl-X ProteinCell LineCell SurvivalDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsExtracellular Signal-Regulated MAP KinasesGATA1 Transcription FactorG-Box Binding FactorsGene Expression RegulationInterleukin-3MAP Kinase Kinase KinasesMiceMitogen-Activated Protein KinasesPhosphorylationBasic-Leucine Zipper Transcription FactorsBcl2l1 protein, mousebcl-X ProteinDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsExtracellular Signal-Regulated MAP KinasesGata1 protein, mouseGATA1 Transcription FactorG-Box Binding FactorsInterleukin-3MAP Kinase Kinase KinasesMitogen-Activated Protein KinasesNfil3 protein, mouseProto-Oncogene Proteins c-bcl-2Transcription Factors

Identifiers

PMID15967790
PMCPMC3193074
OpenAlexW2057137292

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.