Evidence map›Paper›PMID 26150472›Full record

ArticleThe Journal of experimental medicine2015

CCND1-CDK4-mediated cell cycle progression provides a competitive advantage for human hematopoietic stem cells in vivo.

Nicole Mende, Erika E Kuchen, Mathias Lesche, Tatyana Grinenko, Konstantinos D Kokkaliaris, Helmut Hanenberg, Dirk Lindemann, Andreas Dahl, Alexander Platz, Thomas Höfer and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  16. Linking cell cycle to hematopoietic stem cell fate decisions.Frontiers in cell and developmental biology · 2023
    Review
  17. Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022
    Review
  18. Review
  19. Article
  20. Review
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

12 authors at 9 institutions in 5 countries.

Nicole MendeRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Erika E KuchenDivision of Theoretical Systems Biology, German Cancer Research Center, 69120 Heidelberg, Germany Bioquant Center, University of Heidelberg, 69120 Heidelberg, Germany.
Mathias LescheRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Tatyana GrinenkoRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Konstantinos D KokkaliarisDepartment of Biosystems Science and Engineering, ETH Zurich, 4058 Basel, Switzerland.
Helmut HanenbergRiley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN 46202.
Dirk LindemannRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Andreas DahlRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Alexander PlatzDKMS Lifeline Cord Blood Bank, 01277 Dresden, Germany.
Thomas HöferDivision of Theoretical Systems Biology, German Cancer Research Center, 69120 Heidelberg, Germany Bioquant Center, University of Heidelberg, 69120 Heidelberg, Germany.
Federico CalegariRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany.
Claudia WaskowRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Institute of Virology, Center for Regenerative Therapies, Faculty of Medicine; Deep Sequencing Group SFB655, Biotechnology Center, TU Dresden, 01307 Dresden, Germany claudia.waskow@tu-dresden.de.
TU Dresden · DECenter for Neuroscience and Regenerative Medicine · USBerlin-Brandenburger Centrum für Regenerative Therapien · DEETH Zurich · CHGerman Cancer Research Center · DEGerman National Bone Marrow Donor Registry · DEHeidelberg University · DEInstitute of Animal Sciences · CNRiley Hospital for Children · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of stem cell properties is associated with reduced proliferation. However, in mouse hematopoietic stem cells (HSCs), loss of quiescence results in a wide range of phenotypes, ranging from functional failure to extensive self-renewal. It remains unknown whether the function of human HSCs is controlled by the kinetics of cell cycle progression. Using human HSCs and human progenitor cells (HSPCs), we report here that elevated levels of CCND1-CDK4 complexes promoted the transit from G0 to G1 and shortened the G1 cell cycle phase, resulting in protection from differentiation-inducing signals in vitro and increasing human leukocyte engraftment in vivo. Further, CCND1-CDK4 overexpression conferred a competitive advantage without impacting HSPC numbers. In contrast, accelerated cell cycle progression mediated by elevated levels of CCNE1-CDK2 led to the loss of functional HSPCs in vivo. Collectively, these data suggest that the transition kinetics through the early cell cycle phases are key regulators of human HSPC function and important for lifelong hematopoiesis.

Indexed as

Models, BiologicalAnimalsBlotting, WesternCell CycleCell ProliferationCyclin D1Cyclin-Dependent Kinase 4DNA PrimersFlow CytometryGene Transfer TechniquesHematopoietic Stem CellsHigh-Throughput Nucleotide SequencingHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred C57BLCCND1 protein, humanCDK4 protein, humanCyclin D1Cyclin-Dependent Kinase 4DNA Primers

Identifiers

PMID26150472
PMCPMC4516798
OpenAlexW2136769517

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.