Evidence map›Paper›PMID 18346837›Full record

ArticleExperimental hematology2008

Deficiency of Src family kinases compromises the repopulating ability of hematopoietic stem cells.

Christie M Orschell, Jovencio Borneo, Veerendra Munugalavadla, Peilin Ma, Emily Sims, Baskar Ramdas, Mervin C Yoder, Reuben Kapur

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Experimental hematology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. 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. Article
  9. Critical roles of lysosomal acid lipase in myelopoiesis.The American journal of pathology · 2010
    Article
  10. 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

8 authors at 1 institution in 1 country.

Christie M OrschellDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Jovencio Borneo
Veerendra Munugalavadla
Peilin Ma
Emily Sims
Baskar Ramdas
Mervin C Yoder
Reuben Kapur
Indiana University School of Medicine

Funding

Mechanisms of adhesion and growth control in stem cellsR01HL075816 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPUR, REUBEN · 2004 to 2010
$2.3M
Multifaceted Interventions to Amplify HSC EngraftmentR01HL075660 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ORSCHELL, CHRISTIE M · 2005 to 2009
$1.8M
Mechanisms of adhesion and growth control in stem cellsR56HL075816 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2008 to 2008
$378k
NHLBI NIH HHS R01 HL075660NHLBI NIH HHS R01 HL075816NHLBI NIH HHS R01 HL75660NHLBI NIH HHS R56 HL075816
6 · The paper itself

Abstract

objectiveSrc family kinases (SFK) have been implicated in regulating growth factor and integrin-induced proliferation, migration, and gene expression in multiple cell types. However, little is known about the role of these kinases in the growth, homing, and engraftment potential of hematopoietic stem and progenitor cells.

resultsHere we show that loss of hematopoietic-specific SFKs Hck, Fgr, and Lyn results in increased number of Sca-1(+)Lin(-) cells in the bone marrow, which respond differentially to cytokine-induced growth in vitro and manifest a significant defect in the long-term repopulating potential in vivo. Interestingly, a significant increase in expression of adhesion molecules, known to coincide with the homing potential of wild-type bone marrow cells is also observed on the surface of SFK(-/-) cells, although, this increase did not affect the homing potential of more primitive Lin(-)Sca-1(+) SFK(-/-) cells. The stem cell-repopulating defect observed in mice transplanted with SFK(-/-) bone marrow cells is due to the loss of Lyn Src kinase, because deficiency of Lyn, but not Hck or Fgr, recapitulated the long-term stem cell defect observed in mice transplanted with SFK(-/-) bone marrow cells.

conclusionsTaken together, our results demonstrate an essential role for Lyn kinase in positively regulating the long-term and multilineage engraftment of stem cells, which is distinct from its role in mature B cells and myeloid cells.

Indexed as

AnimalsCell DifferentiationCytokinesFlow CytometryHematopoietic Stem CellsMiceMice, CongenicMice, Inbred C57BLMice, KnockoutPhenotypeReproducibility of Resultssrc-Family KinasesStem CellsCytokineslyn protein-tyrosine kinasesrc-Family Kinases

Identifiers

PMID18346837
PMCPMC4378689
OpenAlexW2002434806

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.