Evidence map›Paper›PMID 26884720›Full record

ArticleInternational journal of biological sciences2016

Selective Regulation of MAPK Signaling Mediates RANKL-dependent Osteoclast Differentiation.

Kyunghee Lee, Yeoun Ho Chung, Heejin Ahn, Hyunsoo Kim, Jaerang Rho, Daewon Jeong

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

94 citing papers in PubMed, 166 citations in OpenAlex.

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  18. REGγ is essential to maintain bone homeostasis by degrading TRAF6, preventing osteoporosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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34 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Kyunghee Lee1. Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 705-717, Korea.
Yeoun Ho Chung1. Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 705-717, Korea.
Heejin Ahn1. Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 705-717, Korea.
Hyunsoo Kim1. Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 705-717, Korea.
Jaerang Rho2. Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 305-764, Korea.
Daewon Jeong1. Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine, Daegu 705-717, Korea.
Yeungnam University · KRChungnam National University · KRYeungnam University College

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different stimuli often activate the same intracellular signaling molecules but trigger distinct cell responses. We explored whether or not MAPK signaling induced by macrophage colony-stimulating factor (M-CSF), which is responsible for osteoclast proliferation, differs from that induced by receptor activator of NF-κB ligand (RANKL), which is essential for inducing osteoclast differentiation. The activation of MAPKs by M-CSF or RANKL differed in terms of the extent and duration of ERK, p38, and JNK phosphorylation as well as the isoform specificity of JNK phosphorylation. In particular, RANKL induced a second wave of MAPK activation coincident with the onset of osteoclast differentiation, whereas M-CSF triggered only a monophasic response. M-CSF was also able to trigger a full MAPK response on restimulation of cells earlier than was RANKL, representing that MAPK resensitization by M-CSF differs from that by RANKL. Furthermore, the adapter protein TRAF6 recruitment to the cytoplasmic tail of RANK in a submembrane compartment is specifically required for RANKL-induced activation of p38 MAPK, expression of osteoclastogenic transcription factors, and osteoclast differentiation, indicating that the switch from proliferation to differentiation in osteoclast precursors is dependent on p38 activation via the RANKL-RANK-TRAF6 axis. Our results suggest that selective control of MAPK signaling induced by M-CSF and by RANKL mediates the proliferation versus differentiation decision in osteoclast precursors.

Indexed as

Cell DifferentiationMAP Kinase Signaling SystemAnimalsCell ProliferationGene Expression RegulationMacrophage Colony-Stimulating FactorMaleMice, Inbred C57BLOsteoclastsp38 Mitogen-Activated Protein KinasesPhosphorylationProtein IsoformsRANK LigandTNF Receptor-Associated Factor 6Macrophage Colony-Stimulating Factorp38 Mitogen-Activated Protein KinasesProtein IsoformsRANK LigandTNF Receptor-Associated Factor 6MAPK signalingM-CSFosteoclast differentiationRANKL

Identifiers

PMID26884720
PMCPMC4737679
OpenAlexW2415177601

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.