Evidence map›Paper›PMID 21816924›Full record

ArticleJournal of leukocyte biology2011

A cell-intrinsic role for CaMKK2 in granulocyte lineage commitment and differentiation.

Ellen C Teng, Luigi Racioppi, Anthony R Means

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Impaired CAMK4 Activity Limits Atherosclerosis and Reprograms Myelopoiesis.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Molecular Mechanisms Underlying CaInternational journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Ca(2+)/Calmodulin/CaMKK2 Axis: Nature's Metabolic CaMshaft.Trends in endocrinology and metabolism: TEM · 2016
    Review
  17. Inhibition of Ca²⁺/calmodulin-dependent protein kinase kinase 2 stimulates osteoblast formation and inhibits osteoclast differentiation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013
    Article
  18. Review
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Ellen C TengDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27708, USA.
Luigi Racioppi
Anthony R Means
Duke Medical Center · USDuke University Hospital · US

Funding

STRUCTURE/FUNCTION OF GENETIC ENGINEERED CALMODULINSR01GM033976 · NIGMS · DUKE UNIVERSITY · PI MEANS, ANTHONY R · 1985 to 2015
$5.4M
CaM Kinase Cascades in Endocrine CellsR01DK074701 · NIDDK · DUKE UNIVERSITY · PI MEANS, ANTHONY R · 2006 to 2010
$1.5M
NIDDK NIH HHS R01 DK-074701NIDDK NIH HHS R01 DK074701NIGMS NIH HHS R01 GM033976
6 · The paper itself

Abstract

Granulocytes serve a critical function in host organisms by recognizing and destroying invading microbes, as well as propagating and maintaining inflammation at sites of infection. However, the molecular pathways underpinning the development of granulocytes are poorly understood. Here, we identify a role for CaMKK2 in the restriction of granulocytic fate commitment and differentiation of myeloid progenitor cells. Following BMT, engraftment by Camkk2(-/-) donor cells resulted in the increased production of mature granulocytes in the BM and peripheral blood. Similarly, Camkk2(-/-) mice possessed elevated numbers of CMP cells and exhibited an accelerated granulopoietic phenotype in the BM. Camkk2(-/-) myeloid progenitors expressed increased levels of C/EBPα and PU.1 and preferentially differentiated into Gr1(+)Mac1(+) granulocytes and CFU-G in vitro. During normal granulopoiesis in vivo or G-CSF-induced differentiation of 32D myeloblast cells in vitro, CaMKK2 mRNA and protein were decreased as a function of time and were undetectable in mature granulocytes. Expression of ectopic CaMKK2 in Camkk2(-/-) CMPs was sufficient to rescue aberrant granulocyte differentiation and when overexpressed in 32D cells, was also sufficient to impede granulocyte differentiation in a kinase activity-dependent manner. Collectively, our results reveal a novel role for CaMKK2 as an inhibitor of granulocytic fate commitment and differentiation in early myeloid progenitors.

Indexed as

Cell LineageGranulocytesMyeloid Progenitor CellsAnimalsBone Marrow TransplantationCalcium-Calmodulin-Dependent Protein Kinase KinaseCell DifferentiationCell LineCellular MicroenvironmentCoculture TechniquesLeukocyte Common AntigensMiceStromal CellsWhole-Body IrradiationCalcium-Calmodulin-Dependent Protein Kinase KinaseCamkk2 protein, mouseLeukocyte Common Antigens

Identifiers

PMID21816924
PMCPMC3206468
OpenAlexW2112269591

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.