Evidence map›Paper›PMID 23926327›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Inflammation-mediated notch signaling skews fanconi anemia hematopoietic stem cell differentiation.

Wei Du, Surya Amarachintha, Jared Sipple, Jonathan Schick, Kris Steinbrecher, Qishen Pang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
  6. Neogenin-1 distinguishes between myeloid-biased and balancedProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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

6 authors at 1 institution in 1 country.

Wei DuDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Surya Amarachintha
Jared Sipple
Jonathan Schick
Kris Steinbrecher
Qishen Pang
Cincinnati Children's Hospital Medical Center · US

Funding

Role of FA Proteins in HematopoiesisR01HL076712 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI PANG, QISHEN · 2005 to 2020
$5.0M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Targeted Improvement in Stem Cell Therapy for Leukemia and Bone Marrow Failure SyR01CA157537 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI PANG, QISHEN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA157537NHLBI NIH HHS R01 HL076712NIDDK NIH HHS P30 DK090971
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) can either self-renew or differentiate into various types of cells of the blood lineage. Signaling pathways that regulate this choice of self-renewal versus differentiation are currently under extensive investigation. In this study, we report that deregulation of Notch signaling skews HSC differentiation in mouse models of Fanconi anemia (FA), a genetic disorder associated with bone marrow failure and progression to leukemia and other cancers. In mice expressing a transgenic Notch reporter, deletion of the Fanca or Fancc gene enhances Notch signaling in multipotential progenitors (MPPs), which is correlated with decreased phenotypic long-term HSCs and increased formation of MPP1 progenitors. Furthermore, we found an inverse correlation between Notch signaling and self-renewal capacity in FA hematopoietic stem and progenitor cells. Significantly, FA deficiency in MPPs deregulates a complex network of genes in the Notch and canonical NF-κB pathways. Genetic ablation or pharmacologic inhibition of NF-κB reduces Notch signaling in FA MPPs to near wild type level, and blocking either NF-κB or Notch signaling partially restores FA HSC quiescence and self-renewal capacity. These results suggest a functional crosstalk between Notch signaling and NF-κB pathway in regulation of HSC differentiation.

Indexed as

AnimalsCell DifferentiationDisease Models, AnimalFanconi AnemiaFlow CytometryHematopoietic Stem CellsImmunoblottingInflammationMiceMice, KnockoutNF-kappa BOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionReceptor Cross-TalkReceptors, NotchSignal TransductionNF-kappa BReceptors, Notch

Identifiers

PMID23926327
PMCPMC3773980
OpenAlexW2108003484

What OpenQuestion holds

Textmetadata
LicenceTDM
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.