Evidence map›Paper›PMID 25256217›Full record

ArticleMolecules and cells2014

PKCβ positively regulates RANKL-induced osteoclastogenesis by inactivating GSK-3β.

Jihye Shin, Hyunduk Jang, Jingjing Lin, Soo Young Lee

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Causal relationship between type 2 diabetes mellitus and bone mineral density: a Mendelian randomization study in an East Asian population.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2023
    Article
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  5. Physiologic osteoclasts are not sufficient to induce skeletal pain in mice.European journal of pain (London, England) · 2021
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  7. Review
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  10. Review
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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

4 authors at 1 institution in 1 country.

Jihye ShinDepartment of Life Science and the Research Center for Cellular Home-ostasis, Ewha Womans University, Seoul 120-750, Korea.
Hyunduk JangDepartment of Life Science and the Research Center for Cellular Home-ostasis, Ewha Womans University, Seoul 120-750, Korea ; Present address: Department of Neurology, Seoul National University Hospital, and College of Medicine and Neuroscience Research Institute, Medical Research Center, Seoul National University, Seoul 110-749, Korea.
Jingjing LinDepartment of Life Science and the Research Center for Cellular Home-ostasis, Ewha Womans University, Seoul 120-750, Korea.
Soo Young LeeDepartment of Life Science and the Research Center for Cellular Home-ostasis, Ewha Womans University, Seoul 120-750, Korea.
Ewha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase C (PKC) family members phosphorylate a wide variety of protein targets and are known to be involved in diverse cellular signaling pathways. However, the role of PKC in receptor activator of NF-κB ligand (RANKL) signaling has remained elusive. We now demonstrate that PKCβ acts as a positive regulator which inactivates glycogen synthase kinase-3β (GSK-3β) and promotes NFATc1 induction during RANKL-induced osteoclastogenesis. Among PKCs, PKCβ expression is increased by RANKL. Pharmacological inhibition of PKCβ decreased the formation of osteoclasts which was caused by the inhibition of NFATc1 induction. Importantly, the phosphorylation of GSK-3β was decreased by PKCβ inhibition. Likewise, down-regulation of PKCβ by RNA interference suppressed osteoclast differentiation, NFATc1 induction, and GSK-3β phosphorylation. The administration of PKC inhibitor to the RANKL-injected mouse calvaria efficiently protected RANKL-induced bone destruction. Thus, the PKCβ pathway, leading to GSK-3β inactivation and NFATc1 induction, has a key role in the differentiation of osteoclasts. Our results also provide a further rationale for PKCβ's therapeutic targeting to treat inflammation-related bone diseases.

Indexed as

AnimalsBone ResorptionCell DifferentiationCells, CulturedGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIndolesMaleMaleimidesMiceMice, Inbred C57BLNFATC Transcription FactorsOsteoclastsPhosphorylationProtein Kinase C betaRANK Ligandbisindolylmaleimide IGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseIndolesMaleimidesNfatc1 protein, mouseNFATC Transcription FactorsProtein Kinase C betaRANK LigandRNA, Small Interferingglycogen synthase kinase-3βosteoclast differentiationprotein kinase Cβreceptor activator of NF-κB ligand

Identifiers

PMID25256217
PMCPMC4213766
OpenAlexW2027392443

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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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.