Evidence map›Paper›PMID 36057685›Full record

ArticleNature communications2022

Taz protects hematopoietic stem cells from an aging-dependent decrease in PU.1 activity.

Kyung Mok Kim, Anna Mura-Meszaros, Marie Tollot, Murali Shyam Krishnan, Marco Gründl, Laura Neubert, Marco Groth, Alejo Rodriguez-Fraticelli, Arthur Flohr Svendsen, Stefano Campaner and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. PURE-seq identifiesbioRxiv : the preprint server for biology · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. 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

18 authors at 8 institutions in 5 countries.

Kyung Mok Kim *Transcriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Anna Mura-Meszaros *Transcriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Marie Tollot *Transcriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Murali Shyam KrishnanTranscriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Marco GründlTranscriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.ORCID 0000-0001-5234-4786
Laura NeubertTranscriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Marco GrothLeibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.ORCID 0000-0002-9199-8990
Alejo Rodriguez-FraticelliInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Baldiri Reixac 10, 08028, Barcelona, Spain.ORCID 0000-0002-4017-8714
Arthur Flohr SvendsenLaboratory of Ageing Biology and Stem Cells, European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, Antonius Deusinglaan 1, 9700 AV, Groningen, The Netherlands.ORCID 0000-0002-6224-2334
Stefano CampanerCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Via Adamello 16, 20139, Milan, Italy.ORCID 0000-0003-4547-6849
Nico AndreasInstitute of Immunology, Jena University Hospital, Am Leutragraben 3, 07743, Jena, Germany.
Thomas KamradtInstitute of Immunology, Jena University Hospital, Am Leutragraben 3, 07743, Jena, Germany.
Steve HoffmannLeibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.
Fernando D CamargoInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Baldiri Reixac 10, 08028, Barcelona, Spain.ORCID 0000-0002-5630-5909
Florian H HeidelLeibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany.ORCID 0000-0003-2438-1955
Leonid V BystrykhLaboratory of Ageing Biology and Stem Cells, European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, Antonius Deusinglaan 1, 9700 AV, Groningen, The Netherlands.ORCID 0000-0001-6924-5602
Gerald de HaanLaboratory of Ageing Biology and Stem Cells, European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, Antonius Deusinglaan 1, 9700 AV, Groningen, The Netherlands.ORCID 0000-0001-9706-0138
Björn von EyssTranscriptional Control of Tissue Homeostasis Lab, Leibniz Institute on Aging, Fritz Lipmann Institute e.V., Beutenbergstr. 11, 07745, Jena, Germany. bjoern.voneyss@leibniz-fli.de.ORCID 0000-0002-4731-6841
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEUniversity Medical Center Groningen · NLJena University Hospital · DEBoston Children's Hospital · USInstitute for Research in Biomedicine · ESItalian Institute of Technology · ITLeibniz Association · DEUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specific functions of the immune system are essential to protect us from infections caused by pathogens such as viruses and bacteria. However, as we age, the immune system shows a functional decline that can be attributed in large part to age-associated defects in hematopoietic stem cells (HSCs)-the cells at the apex of the immune cell hierarchy. Here, we find that the Hippo pathway coactivator TAZ is potently induced in old HSCs and protects these cells from functional decline. We identify Clca3a1 as a TAZ-induced gene that allows us to trace TAZ activity in vivo. Using CLCA3A1 as a marker, we can isolate "young-like" HSCs from old mice. Mechanistically, Taz acts as coactivator of PU.1 and to some extent counteracts the gradual loss of PU.1 expression during HSC aging. Our work thus uncovers an essential role for Taz in a previously undescribed fail-safe mechanism in aging HSCs.

Indexed as

AgingHematopoietic Stem CellsAnimalsMice

Identifiers

PMID36057685
PMCPMC9440927
OpenAlexW4294368752

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.