Evidence map›Paper›PMID 24264602›Full record

ArticleJournal of cellular physiology2014

ERK5 pathway regulates transcription factors important for monocytic differentiation of human myeloid leukemia cells.

Xuening Wang, Stella Pesakhov, Jonathan S Harrison, Michael Danilenko, George P Studzinski

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Exposure toBioMed research international · 2016
    Article
  14. Article
  15. Review
  16. Article
  17. Inhibition of ERK5 enhances cytarabine-induced apoptosis in acute myeloid leukemia cells.International journal of clinical and experimental medicine · 2015
    Article
  18. 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

5 authors at 3 institutions in 2 countries.

Xuening WangDepartment of Pathology and Laboratory Medicine, Rutgers Biomedical and Health Sciences, Newark, New Jersey.
Stella Pesakhov
Jonathan S Harrison
Michael Danilenko
George P Studzinski
Ben-Gurion University of the Negev · ILRutgers, The State University of New Jersey · USJohnson University · US

Funding

Vitamin D Analogs as Adjuvants in Chemotherapy of CancerR01CA044722 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI STUDZINSKI, GEORGE P · 1987 to 2016
$3.5M
NCI NIH HHS 5R01CA44722-22NCI NIH HHS R01 CA044722
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) are important transducers of external signals for cell growth, survival, and other cellular responses including cell differentiation. Several MAPK cascades are known with the MEK1/2-ERK1/2, JNK, and p38MAPKs receiving most attention, but the role of MEK5-ERK5 in intracellular signaling deserves more scrutiny, as this pathway transmits signals that can complement ERK/2 signaling. We hypothesized that the ERK5 pathway plays a role in the control of monocytic differentiation, which is disturbed in myeloid leukemia. We therefore examined the cellular phenotype and key molecular events which occur when human myeloid leukemia cells, acute (AML) or chronic (CML), are forced to differentiate by vitamin D derivatives (VDDs). This study was performed using established cell lines HL60 and U937, and primary cultures of blasts from 10 patients with ML. We found that ERK5 and its direct downstream target transcription factor MEF2C are upregulated by 1,25D in parallel with monocytic differentiation. Further, inhibition of ERK5 activity by specific pharmacological agents BIX02189 and XMD8-92 alters the phenotype of these cells by reducing the abundance of the VDD-induced surface monocytic marker CD14, and concomitantly increasing surface expression of the general myeloid marker CD11b. Similar results were obtained when the expression of ERK5 was reduced by siRNA or short hairpin (sh) RNA. ERK5 inhibition resulted in an expected decrease in MEF2C activation. We also found that in AML cells the transcription factor C/EBPβ is positively regulated, while C/EBPα is negatively regulated by ERK5. These findings provide new understanding of dysregulated differentiation in human myeloid leukemia.

Indexed as

Aniline CompoundsBenzodiazepinonesCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding ProteinsCell DifferentiationGene Expression Regulation, NeoplasticHL-60 CellsHumansIndolesLeukemia, MyeloidMEF2 Transcription FactorsMitogen-Activated Protein Kinase 7MonocytesSignal TransductionTranscription FactorsU937 CellsAniline CompoundsBenzodiazepinonesBIX 02189CCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding ProteinsCEBPB protein, humanIndolesMEF2C protein, humanMEF2 Transcription FactorsMitogen-Activated Protein Kinase 7Transcription FactorsVitamin DXMD 8-92

Identifiers

PMID24264602
PMCPMC4363988
OpenAlexW2159201625

What OpenQuestion holds

Textmetadata
LicenceTDM
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.