Evidence map›Paper›PMID 25451916›Full record

ArticleThe Journal of biological chemistry2015

Choline kinase β mutant mice exhibit reduced phosphocholine, elevated osteoclast activity, and low bone mass.

Jasreen Kular, Jennifer C Tickner, Nathan J Pavlos, Helena M Viola, Tamara Abel, Bay Sie Lim, Xiaohong Yang, Honghui Chen, Robert Cook, Livia C Hool and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Preclinical efficacy of a gene therapy forMolecular therapy. Advances · 2026
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  10. Role of Metabolism in Bone Development and Homeostasis.International journal of molecular sciences · 2020
    Review
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  17. Review
  18. Deficiency in Fpr2 results in reduced numbers of LinThe Journal of biological chemistry · 2018
    Article
  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

12 authors at 2 institutions in 2 countries.

Jasreen KularFrom the School of Pathology and Laboratory Medicine.
Jennifer C TicknerFrom the School of Pathology and Laboratory Medicine.
Nathan J PavlosCentre for Orthopaedic Research, School of Surgery.
Helena M ViolaSchool of Anatomy, Physiology and Human Biology, and.
Tamara AbelCentre for Microscopy, Characterization and Analysis, University of Western Australia, Nedlands 6009, Western Australia, Australia and.
Bay Sie LimFrom the School of Pathology and Laboratory Medicine.
Xiaohong Yangthe Guangzhou Institute of Traumatic Surgery, the Fourth Affiliated Hospital of Medical College, Jinan University, Guangzhou 510182, China.
Honghui Chenthe Guangzhou Institute of Traumatic Surgery, the Fourth Affiliated Hospital of Medical College, Jinan University, Guangzhou 510182, China.
Robert CookFrom the School of Pathology and Laboratory Medicine.
Livia C HoolSchool of Anatomy, Physiology and Human Biology, and.
Ming Hao ZhengCentre for Orthopaedic Research, School of Surgery.
Jiake XuFrom the School of Pathology and Laboratory Medicine, jiake.xu@uwa.edu.au.
University of Western Australia · AUJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The maintenance of bone homeostasis requires tight coupling between bone-forming osteoblasts and bone-resorbing osteoclasts. However, the precise molecular mechanism(s) underlying the differentiation and activities of these specialized cells are still largely unknown. Here, we identify choline kinase β (CHKB), a kinase involved in the biosynthesis of phosphatidylcholine, as a novel regulator of bone homeostasis. Choline kinase β mutant mice (flp/flp) exhibit a systemic low bone mass phenotype. Consistently, osteoclast numbers and activity are elevated in flp/flp mice. Interestingly, osteoclasts derived from flp/flp mice exhibit reduced sensitivity to excessive levels of extracellular calcium, which could account for the increased bone resorption. Conversely, supplementation of cytidine 5'-diphosphocholine in vivo and in vitro, a regimen that bypasses CHKB deficiency, restores osteoclast numbers to physiological levels. Finally, we demonstrate that, in addition to modulating osteoclast formation and function, loss of CHKB corresponds with a reduction in bone formation by osteoblasts. Taken together, these data posit CHKB as a new modulator of bone homeostasis.

Indexed as

MutationAnimalsBone and BonesBone DensityBone ResorptionCalciumCell ProliferationCholine KinaseHomeostasisMiceMice, TransgenicMicroscopy, FluorescenceMutagenesisOsteoblastsOsteoclastsPhenotypeCalciumCholine KinasePhosphorylcholineBoneCholine Kinase-βMutagenesisOsteoblastOsteoclastOsteoporosis

Identifiers

PMID25451916
PMCPMC4340415
OpenAlexW2312364251

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.