Evidence map›Paper›PMID 17536016›Full record

ArticleBlood2007

Activation of mitogen-activated protein kinase kinase (MEK)/extracellular signal regulated kinase (ERK) signaling pathway is involved in myeloid lineage commitment.

Chia-Lin Hsu, Kazu Kikuchi, Motonari Kondo

Abstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Frontiers in cell and developmental biology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Signal, transduction, and the hematopoietic stem cell.Rambam Maimonides medical journal · 2014
    Article
  19. Review
  20. 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

3 authors.

Chia-Lin HsuDepartment of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
Kazu Kikuchi
Motonari Kondo

Funding

IL-7 receptor signaling in lymphopoiesisR01AI056123 · NIAID · DUKE UNIVERSITY · PI KONDO, MOTONARI · 2004 to 2010
$2.1M
Commitment mechanisms in hemato/lymphopoiesisR01CA098129 · NCI · DUKE UNIVERSITY · PI KONDO, MOTONARI · 2004 to 2008
$1.4M
NCI NIH HHS CA098129NCI NIH HHS R01 CA098129NIAID NIH HHS AI056123NIAID NIH HHS R01 AI056123
6 · The paper itself

Abstract

Common lymphoid progenitors (CLPs) are lymphoid-lineage-committed progenitor cells. However, they maintain a latent myeloid differentiation potential that can be initiated by stimulation with interleukin-2 (IL-2) via ectopically expressed IL-2 receptors. Although CLPs express IL-7 receptors, which share the common gamma chain with IL-2 receptors, IL-7 cannot initiate lineage conversion in CLPs. In this study, we demonstrate that the critical signals for initiating lineage conversion in CLPs are delivered via IL-2 receptor beta (IL-2R beta) intracellular domains. Fusion of the A region of the IL-2R beta cytoplasmic tail to IL-7R alpha enables IL-7 to initiate myeloid differentiation in CLPs. We found that Shc, which associates with the A region, mediates lineage conversion signals through the mitogen activated protein kinase (MAPK) pathway. Because mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitors completely blocked IL-2-mediated lineage conversion, MAPK activation, specifically via the MEK/ERK pathway, is critically involved in the initiation of this event. Furthermore, formation of granulocyte/macrophage (GM) colonies by hematopoietic stem cells, but not by common myeloid progenitors (CMPs), was severely reduced in the presence of MEK/ERK inhibitors. These results demonstrate that activation of MEK/ERK plays an important role in GM lineage commitment.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell DifferentiationCells, CulturedExtracellular Signal-Regulated MAP KinasesInterleukin-2Interleukin-2 Receptor beta SubunitLymphocytesMiceMyeloid Progenitor CellsProtein Kinase InhibitorsProtein Structure, TertiaryReceptors, Interleukin-7Recombinant Fusion ProteinsShc Signaling Adaptor ProteinsSignal TransductionAdaptor Proteins, Signal TransducingExtracellular Signal-Regulated MAP KinasesIl2rb protein, mouseInterleukin-2Interleukin-2 Receptor beta SubunitProtein Kinase InhibitorsReceptors, Interleukin-7Recombinant Fusion ProteinsShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID17536016
PMCPMC1975832

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.