Evidence map›Paper›PMID 17702896›Full record

ArticleBlood2007

Cdc42 critically regulates the balance between myelopoiesis and erythropoiesis.

Linda Yang, Lei Wang, Theodosia A Kalfa, Jose A Cancelas, Xun Shang, Suvarnamala Pushkaran, Jun Mo, David A Williams, Yi Zheng

Open access · bronzeAbstract 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 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

61 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Science advances · 2023
    Article
  7. Article
  8. Article
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  10. Article
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  14. Article
  15. Review
  16. Article
  17. Article
  18. A New Patient with NOCARH Syndrome Due to CDC42 Defect.Journal of clinical immunology · 2020
    Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Linda YangDivision of Experimental Hematology, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Lei Wang
Theodosia A Kalfa
Jose A Cancelas
Xun Shang
Suvarnamala Pushkaran
Jun Mo
David A Williams
Yi Zheng
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Cell Type and Stimulus-Specific Signaling Role of CDC42 in BloodR01HL085362 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2006 to 2010
$2.0M
Rho GTPase-Activating Proteins in CancerR01CA105117 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2004 to 2008
$1.2M
NCI NIH HHS R01 CA105117NHLBI NIH HHS R01 HL085362
6 · The paper itself

Abstract

The Rho GTPase Cdc42 regulates adhesion, migration, and homing, as well as cell cycle progression, of hematopoietic stem cells, but its role in multilineage blood development remains unclear. We report here that inducible deletion of cdc42 in cdc42-floxed mouse bone marrow by the interferon-responsive, Mx1-Cre-mediated excision led to myeloid and erythroid developmental defects. Cdc42 deletion affected the number of early myeloid progenitors while suppressing erythroid differentiation. Cdc42-deficient mice developed a fatal myeloproliferative disorder manifested by significant leukocytosis with neutrophilia, myeloid hyperproliferation, and myeloid cell infiltration into distal organs. Concurrently, Cdc42 deficiency caused anemia and splenomegaly accompanied with decreased bone marrow erythroid burst-forming units (BFU-Es) and colony-forming units-erythroid (CFU-Es) activities and reduced immature erythroid progenitors, suggesting that Cdc42 deficiency causes a block in the early stage of erythropoiesis. Cdc42 activity is responsive to stimulation by SCF, IL3, SDF-1alpha, and fibronectin. The increased myelopoiesis and decreased erythropoiesis of the knockout mice are associated with an altered gene transcription program in hematopoietic progenitors, including up-regulation of promyeloid genes such as PU.1, C/EBP1alpha, and Gfi-1 in the common myeloid progenitors and granulocyte-macrophage progenitors and down-regulation of proerythroid gene such as GATA-2 in the megakaryocyte-erythroid progenitors. Thus, Cdc42 is an essential regulator of the balance between myelopoiesis and erythropoiesis.

Indexed as

ErythropoiesisGene Expression Regulation, EnzymologicMyelopoiesisAnemiaAnimalsCCAAT-Enhancer-Binding Proteinscdc42 GTP-Binding ProteinCell AdhesionCell MovementCell ProliferationChemokine CXCL12DNA-Binding ProteinsErythroid Precursor CellsFibronectinsGATA2 Transcription FactorGene DeletionCCAAT-Enhancer-Binding Proteinscdc42 GTP-Binding ProteinChemokine CXCL12DNA-Binding ProteinsFibronectinsGata2 protein, mouseGATA2 Transcription FactorGfi1 protein, mouseInterleukin-3Proto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTranscription Factors

Identifiers

PMID17702896
PMCPMC2190607
OpenAlexW2066021681

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.