Evidence map›Paper›PMID 26282877›Full record

ArticleThe Journal of experimental medicine2015

Kindlin-3-mediated integrin adhesion is dispensable for quiescent but essential for activated hematopoietic stem cells.

Raphael Ruppert, Markus Moser, Markus Sperandio, Emanuel Rognoni, Martin Orban, Wen-Hsin Liu, Ansgar S Schulz, Robert A J Oostendorp, Steffen Massberg, Reinhard Fässler

Abstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. ICAP-1 loss impairs CD8European journal of immunology · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Kindlin-3 loss curbs chronic myeloid leukemia in mice by mobilizing leukemic stem cells from protective bone marrow niches.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Role of Kindlin-2 in cancer progression and metastasis.Annals of translational medicine · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Bone marrow laminins influence hematopoietic stem and progenitor cell cycling and homing to the bone marrow.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Raphael RuppertDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Markus MoserDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Markus SperandioWalter Brendel Center of Experimental Medicine, Ludwig Maximilian University, 80539 Munich, Germany.
Emanuel RognoniDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Martin OrbanMedical Clinic and Policlinic I, Klinikum der Universität, 80336 Munich, Germany.
Wen-Hsin LiuDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Ansgar S SchulzDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, 89081 Ulm, Germany.
Robert A J OostendorpThird Department of Internal Medicine, Klinikum rechts der Isar, Technische Universität, 80337 Munich, Germany.
Steffen MassbergMedical Clinic and Policlinic I, Klinikum der Universität, 80336 Munich, Germany.
Reinhard FässlerDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany faessler@biochem.mpg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) generate highly dividing hematopoietic progenitor cells (HPCs), which produce all blood cell lineages. HSCs are usually quiescent, retained by integrins in specific niches, and become activated when the pools of HPCs decrease. We report that Kindlin-3-mediated integrin activation controls homing of HSCs to the bone marrow (BM) and the retention of activated HSCs and HPCs but not of quiescent HSCs in their BM niches. Consequently, Kindlin-3-deficient HSCs enter quiescence and remain in the BM when cotransplanted with wild-type hematopoietic stem and progenitor cells (HSPCs), whereas they are hyperactivated and lost in the circulation when wild-type HSPCs are absent, leading to their exhaustion and reduced survival of recipients. The accumulation of HSPCs in the circulation of leukocyte adhesion deficiency type III patients, who lack Kindlin-3, underlines the conserved functions of Kindlin-3 in man and the importance of our findings for human disease.

Indexed as

AnimalsBone MarrowCell AdhesionCytoskeletal ProteinsFemaleHematopoietic Stem CellsHumansInfantIntegrinsMaleMembrane ProteinsMiceMice, KnockoutNeoplasm ProteinsCytoskeletal ProteinsFERMT3 protein, humanIntegrinskindlin-3 protein, mouseMembrane ProteinsNeoplasm Proteins

Identifiers

PMID26282877
PMCPMC4548061

What OpenQuestion holds

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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.