Evidence map›Paper›PMID 16467205›Full record

ArticleBlood2006

Integrin inhibition through Lyn-dependent cross talk from CXCR4 chemokine receptors in normal human CD34+ marrow cells.

Yuji Nakata, Brian Tomkowicz, Alan M Gewirtz, Andrzej Ptasznik

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. IL-1β and CXCR4 as Potential Therapeutic Targets for Alzheimer's Disease.Combinatorial chemistry & high throughput screening · 2025
    Article
  4. Loss of Function of DOCK4 in Myelodysplastic Syndromes Stem Cells is Restored by Inhibitors of DOCK4 Signaling Networks.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Essential Role of Lyn in Fibrosis.Frontiers in physiology · 2016
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  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 1 institution in 1 country.

Yuji NakataDepartment of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Brian Tomkowicz
Alan M Gewirtz
Andrzej Ptasznik
University of Pennsylvania · US

Funding

Developing Nucleic Acid TherapeuticsR01CA101859 · NCI · UNIVERSITY OF PENNSYLVANIA · PI GEWIRTZ, ALAN M · 2003 to 2007
$1.4M
Crosstalk between oncoprotein and chemokine signalingR01CA108552 · NCI · UNIVERSITY OF PENNSYLVANIA · PI PTASZNIK, ANDRZEJ · 2005 to 2007
$698k
NCI NIH HHS 1R01CA108 552-01A1NCI NIH HHS R01CA101 859
6 · The paper itself

Abstract

We studied the effects of Lyn ablation on CXCR4 receptor-mediated migration and adhesion of hematopoietic precursors. Down-regulation of Lyn expression with siRNA greatly reduced CXCR4-dependent hematopoietic cell movement, and increased cell adherence to stroma. This increase was associated with the up-regulated expression of activation-dependent epitopes of the beta(2) integrin LFA-1 and was prevented by antibodies that selectively block cell adhesion mediated by ICAM-1. Attachment to surfaces coated with ICAM-1 was also enhanced in Lyn-depleted hematopoietic cells, as compared with Lyn-expressing cells. Functional rescue experiments with Lyn siRNA targeting the 3' UTR indicated that the observed effects can be attributed directly to specific inhibition of Lyn. Our results show that in chemokine-stimulated hematopoietic cells Lyn kinase is a positive regulator of cell movement while negatively regulating adhesion to stromal cells by inhibiting the ICAM-1-binding activity of beta(2) integrins. These results provide a molecular mechanism for cross talk between the chemokine receptor CXCR4 and beta(2) integrins. This cross talk may allow chemokine receptors to modulate the arrest of rolling hematopoietic precursors on the surface of bone marrow stromal cells.

Indexed as

Receptor Cross-TalkAntigens, CD34Bone Marrow CellsCD18 AntigensCell AdhesionCell MovementCells, CulturedHematopoietic Stem CellsHumansIntegrinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Receptors, CXCR4RNA, Small Interferingsrc-Family KinasesStromal CellsAntigens, CD34CD18 AntigensIntegrinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1lyn protein-tyrosine kinaseReceptors, CXCR4RNA, Small Interferingsrc-Family Kinases

Identifiers

PMID16467205
PMCPMC1895784
OpenAlexW2069115610

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.