Evidence map›Paper›PMID 18579797›Full record

ArticleBlood2008

Rac GTPase isoforms Rac1 and Rac2 play a redundant and crucial role in T-cell development.

Fukun Guo, Jose A Cancelas, David Hildeman, David A Williams, Yi Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025
    Review
  8. Article
  9. Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. RhoG's Role in T Cell Activation and Function.Frontiers in immunology · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. The DNA-helicase HELLS drives ALKCell death & disease · 2021
    Article
  20. Article

7 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

5 authors at 2 institutions in 1 country.

Fukun GuoDivision of Experimental Hematology and Cancer Biology, Children's Hospital Medical Center, OH, USA.
Jose A Cancelas
David Hildeman
David A Williams
Yi Zheng
Children's Hospital & Medical Center · USUniversity of Cincinnati · US

Funding

Rac proteins in hematopoietic cell survival and functionR01DK062757 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLIAMS, DAVID A · 2002 to 2016
$5.7M
Regulation of Apoptosis in Activated Primary T CellsR01AI057753 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HILDEMAN, DAVID A · 2005 to 2013
$2.8M
Rac GTPases as Targets in LymphomagenesisR01CA125658 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2007 to 2011
$2.1M
INTERACTION OF RHO GTPASES WITH REGULATORS AND EFFECTORSR01GM060523 · NIGMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHENG, YI · 2000 to 2007
$1.9M
NCI NIH HHS R01 CA125658NIAID NIH HHS R01 AI057753NIDDK NIH HHS R01 DK062757NIDDK NIH HHS R01 DK62757NIGMS NIH HHS R01 GM060523NIGMS NIH HHS R01 GM60523
6 · The paper itself

Abstract

Rac GTPases have been implicated in the regulation of diverse functions in various blood cell lineages, but their role in T-cell development is not well understood. We have carried out conditional gene targeting to achieve hematopoietic stem cell (HSC)- or T-cell lineage-specific deletion of Rac1 or Rac1/Rac2 by crossbreeding the Mx-Cre or Lck-Cre transgenic mice with Rac1(loxp/loxp) or Rac1(loxp/loxp);Rac2(-/-) mice. We found that (1) HSC deletion of both Rac1 and Rac2 inhibited production of common lymphoid progenitors (CLPs) in bone marrow and suppressed T-cell development in thymus and peripheral organs, whereas deletion of Rac1 moderately affected CLP production and T-cell development. (2) T cell-specific deletion of Rac1 did not affect T-cell development, whereas deletion of both Rac1 and Rac2 reduced immature CD4(+)CD8(+) and mature CD4(+) populations in thymus as well as CD4(+) and CD8(+) populations in spleen. (3) The developmental defects of Rac1/Rac2 knockout T cells were associated with proliferation, survival, adhesion, and migration defects. (4) Rac1/Rac2 deletion suppressed T-cell receptor-mediated proliferation, IL-2 production, and Akt activation in thymocytes. Thus, Rac1 and Rac2 have unique roles in CLP production and share a redundant but essential role in later stages of T-cell development by regulating survival and proliferation signals.

Indexed as

AnimalsCell DifferentiationCell MovementCell ProliferationCell SurvivalGene TargetingHematopoietic Stem CellsInterleukin-2LymphopoiesisMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeuropeptidesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinInterleukin-2NeuropeptidesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinRac1 protein, mouseRAC2 GTP-Binding Proteinrac GTP-Binding ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID18579797
PMCPMC2518885
OpenAlexW2012300995

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.