Evidence map›Paper›PMID 16174757›Full record

ArticleBlood2006

Genetic deletion of Cdc42GAP reveals a role of Cdc42 in erythropoiesis and hematopoietic stem/progenitor cell survival, adhesion, and engraftment.

Lei Wang, Linda Yang, Marie-Dominique Filippi, David A Williams, Yi Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Human erythrocytes: cytoskeleton and its origin.Cellular and molecular life sciences : CMLS · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. RNA-binding proteins mind the GAPs.Nature immunology · 2017
    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 1 institution in 1 country.

Lei WangDivision of Experimental Hematology, Children's Hospital Medical Center, University of Cincinnati, OH 45229, USA.
Linda Yang
Marie-Dominique Filippi
David A Williams
Yi Zheng
Hospital Research Foundation · AU

Funding

Rac proteins in hematopoietic cell survival and functionR01DK062757 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLIAMS, DAVID A · 2002 to 2016
$5.7M
Dbl-like Regulators of Small GTP-binding ProteinsR01GM053943 · NIGMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHENG, YI · 1996 to 2008
$2.3M
Rho GTPase-Activating Proteins in CancerR01CA105117 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2004 to 2008
$1.2M
NCI NIH HHS R01 CA105117NIDDK NIH HHS R01 DK062757NIDDK NIH HHS R01DK62757NIGMS NIH HHS R01 GM53943
6 · The paper itself

Abstract

Rho family GTPases are key signal transducers in cell regulation. Although a body of literature has implicated the Rho family members Rac1 and Rac2 in multiple hematopoietic-cell functions, the role of Cdc42 in hematopoiesis remains unclear. Here we have examined the hematopoietic properties and the hematopoietic stem/progenitor cell (HSP) functions of gene-targeted mice carrying null alleles of cdc42gap, a negative regulator of Cdc42. The Cdc42GAP-/- fetal liver and bone marrow cells showed a 3-fold increase in Cdc42 activity but normal Rac and RhoA activities, indicating that Cdc42GAP knockout resulted in a gain of Cdc42 activity in the hematopoietic tissues. Cdc42GAP-/- mice were anemic. The cellularity of fetal liver and bone marrow, the number and composition percentage of HSPs, and the erythroid blast-forming unit and colony-forming unit (BFU-E/CFU-E) activities were significantly reduced in the homozygous mice. The decrease in HSP number was associated with increased apoptosis of the Cdc42GAP-/- HSPs and the activation of JNK-mediated apoptotic machinery. Moreover, homozygous HSPs showed impaired cortical F-actin assembly, deficiency in adhesion and migration, and defective engraftment. These results provide evidence that Cdc42 activity is important for erythropoiesis and for multiple HSP functions, including survival, adhesion, and engraftment.

Indexed as

ErythropoiesisActinsAnemiaAnimalsApoptosiscdc42 GTP-Binding ProteinCell AdhesionCell CountCell SurvivalGene DeletionGraft SurvivalHematopoiesisHematopoietic Stem CellsMiceMice, KnockoutActinscdc42 GTP-Binding Protein

Identifiers

PMID16174757
PMCPMC1895350
OpenAlexW1974896636

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.