Evidence map›Paper›PMID 19671922›Full record

ArticleBlood2009

Rho GTPase Cdc42 is essential for B-lymphocyte development and activation.

Fukun Guo, Chinavenmeni S Velu, H Leighton Grimes, Yi Zheng

Open access · greenAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. ImmunoHorizons · 2020
    Article
  7. A New Patient with NOCARH Syndrome Due to CDC42 Defect.Journal of clinical immunology · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Small Rho GTPase TC10 Modulates B Cell Immune Responses.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  17. Article
  18. Review
  19. Article
  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

4 authors at 2 institutions in 1 country.

Fukun GuoDivision of Experimental Hematology, Children's Hospital Research Foundation, University of Cincinnati, OH 45229, USA.
Chinavenmeni S Velu
H Leighton Grimes
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

Cdc42 is a member of the Rho GTPase family that has been implicated in several cell functions including proliferation and migration, but its physiologic role needs to be dissected in each cell type. We achieved B-cell and hematopoietic stem cell deletion of Cdc42 by conditional gene targeting in mice. Deletion of Cdc42 from proB/preB-cell stage significantly blocked B-cell development at T1 and later stages, resulting in reduced mature B-cell populations and reduced antigen-specific immunoglobulin M (IgM), IgG1, and IgG3 production. The Cdc42(-/-) B cells, themselves, were abnormal with impaired proliferation and survival. The mutant B cells were further characterized by a B-cell receptor (BCR) signaling defect with increased Erk and decreased Akt activation, as well as a defect in BCR-mediated B-cell-activating factor (BAFF) receptor up-regulation and subsequent BAFF receptor signaling in mature resting B cells. Surprisingly, Cdc42 was dispensable for stromal cell-derived factor-1alpha (SDF-1alpha)- or B-lymphocyte chemoattractant (BLC)-induced B-cell migration. Finally, loss of Cdc42 from hematopoietic stem cells did not alter common lymphoid progenitor production but severely reduced proB/preB- and immature B-cell populations, indicating that Cdc42 is also involved in B-cell precursor differentiation. These results reveal multifaceted roles of Cdc42 in B-cell development and activation.

Indexed as

Lymphocyte ActivationAnimalsB-Cell Activation Factor ReceptorBlotting, WesternB-Lymphocytescdc42 GTP-Binding ProteinCell DifferentiationCell MovementCell ProliferationChemokine CXCL12Enzyme-Linked Immunosorbent AssayGene Expression ProfilingHematopoietic Stem CellsImmunoglobulin GImmunoglobulin MIntegrasesB-Cell Activation Factor Receptorcdc42 GTP-Binding ProteinChemokine CXCL12Cre recombinaseImmunoglobulin GImmunoglobulin MIntegrasesReceptors, Antigen, B-Cell

Identifiers

PMID19671922
PMCPMC2756201
OpenAlexW1973286130

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.