Evidence map›Paper›PMID 19369945›Full record

ArticleThe EMBO journal2009

MAPKAP kinase MK2 maintains self-renewal capacity of haematopoietic stem cells.

Jessica Schwermann, Chozhavendan Rathinam, Maria Schubert, Stefanie Schumacher, Fatih Noyan, Haruhiko Koseki, Alexey Kotlyarov, Christoph Klein, Matthias Gaestel

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Sticky, Adaptable, and Many-sided: SAM protein versatility in normal and pathological hematopoietic states.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
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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

9 authors at 2 institutions in 2 countries.

Jessica SchwermannInstitute of Biochemistry, Hannover Medical School, Hannover, Germany.
Chozhavendan Rathinam
Maria Schubert
Stefanie Schumacher
Fatih Noyan
Haruhiko Koseki
Alexey Kotlyarov
Christoph Klein
Matthias Gaestel
Medizinische Hochschule Hannover · DERIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The structurally related MAPK-activated protein kinases (MAPKAPKs or MKs) MK2, MK3 and MK5 are involved in multiple cellular functions, including cell-cycle control and cellular differentiation. Here, we show that after deregulation of cell-cycle progression, haematopoietic stem cells (HSCs) in MK2-deficient mice are reduced in number and show an impaired ability for competitive repopulation in vivo. To understand the underlying molecular mechanism, we dissected the role of MK2 in association with the polycomb group complex (PcG) and generated a MK2 mutant, which is no longer able to bind to PcG. The reduced ability for repopulation is rescued by re-introduction of MK2, but not by the Edr2-non-binding mutant of MK2. Thus, MK2 emerges as a regulator of HSC homeostasis, which could act through chromatin remodelling by the PcG complex.

Indexed as

AnimalsGenetic Complementation TestHematopoietic Stem CellsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MiceMice, Inbred C57BLMice, KnockoutPolycomb-Group ProteinsProtein BindingProtein Serine-Threonine KinasesRepressor ProteinsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Polycomb-Group ProteinsProtein Serine-Threonine KinasesRepressor Proteins

Identifiers

PMID19369945
PMCPMC2688528
OpenAlexW2113884444

What OpenQuestion holds

Textmetadata
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.