Evidence map›Paper›PMID 27503415›Full record

ArticleScientific reports2016

Quantitative trait gene Slit2 positively regulates murine hematopoietic stem cell numbers.

Amanda Waterstrat, Kyle Rector, Hartmut Geiger, Ying Liang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Adult haematopoietic stem cell niches.Nature reviews. Immunology · 2017
    Review
  4. 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 3 institutions in 2 countries.

Amanda WaterstratDivision of Mathematics and Natural Sciences, Somerset Community College, Laurel Campus, London, KY, USA.
Kyle RectorDepartment of Physiology, University of Kentucky, Lexington, KY, USA.
Hartmut GeigerDivision of Experimental Hematology and Cancer Biology, Children's Hospital Medical Center, Cincinnati, OH, USA.
Ying LiangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, USA.
University of Kentucky · USSomerset Community College · USUniversity Hospital Ulm · DE

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
Latexin function in the maintenance and regeneration of the hematopoietic systemR01HL124015 · NHLBI · UNIVERSITY OF KENTUCKY · PI LIANG, YING · 2016 to 2024
$3.6M
Kentucky Center for Clinical and Translational ScienceKL2TR000116 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$1.9M
Research Training in Muscle Biology of Cardiopulmonary DiseaseT32HL086341 · NHLBI · UNIVERSITY OF KENTUCKY · PI ANDRADE, FRANCISCO H · 2008 to 2012
$610k
Genetic Regulation of Hematopoietic Stem Cell NumberR36AG029669 · NIA · UNIVERSITY OF KENTUCKY · PI WATERSTRAT, AMANDA JO · 2007 to 2008
$62k
NCATS NIH HHS KL2 TR000116NCATS NIH HHS UL1 TR000117NCI NIH HHS P30 CA177558NHLBI NIH HHS R01 HL124015NHLBI NIH HHS T32 HL086341NIA NIH HHS R36 AG029669
6 · The paper itself

Abstract

Hematopoietic stem cells (HSC) demonstrate natural variation in number and function. The genetic factors responsible for the variations (or quantitative traits) are largely unknown. We previously identified a gene whose differential expression underlies the natural variation of HSC numbers in C57BL/6 (B6) and DBA/2 (D2) mice. We now report the finding of another gene, Slit2, on chromosome 5 that also accounts for variation in HSC number. In reciprocal chromosome 5 congenic mice, introgressed D2 alleles increased HSC numbers, whereas B6 alleles had the opposite effect. Using gene array and quantitative polymerase chain reaction, we identified Slit2 as a quantitative trait gene whose expression was positively correlated with the number of HSCs. Ectopic expression of Slit2 not only increased the number of the long-term colony forming HSCs, but also enhanced their repopulation capacity upon transplantation. Therefore, Slit2 is a novel quantitative trait gene and a positive regulator of the number and function of murine HSCs. This finding suggests that Slit2 may be a potential therapeutic target for the effective in vitro and in vivo expansion of HSCs without compromising normal hematopoiesis.

Indexed as

AnimalsGene Expression RegulationHematopoietic Stem CellsIntercellular Signaling Peptides and ProteinsMiceMice, CongenicMice, Inbred C57BLMice, Inbred DBANerve Tissue ProteinsQuantitative Trait LociSlit Homolog 2 ProteinIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsSlit Homolog 2 Protein

Identifiers

PMID27503415
PMCPMC4977545
OpenAlexW2527376409

What OpenQuestion holds

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LicenceCC BY
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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.