Evidence map›Paper›PMID 30142160›Full record

ArticlePLoS biology2018

A dual-specific macrophage colony-stimulating factor antagonist of c-FMS and αvβ3 integrin for osteoporosis therapy.

Yuval Zur, Lior Rosenfeld, Chen Anna Keshelman, Nofar Dalal, Gali Guterman-Ram, Ayelet Orenbuch, Yulia Einav, Noam Levaot, Niv Papo

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2018. 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
1.9field-weighted citation impact, top 16% 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, 26 citations in OpenAlex.

  1. Review
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  13. Article
  14. The M-CSF receptor in osteoclasts and beyond.Experimental & molecular medicine · 2020
    Review
  15. Article
  16. Article
  17. Modulation of αActa histochemica et cytochemica · 2019
    Article
  18. Non-Viral Delivery System and Targeted Bone Disease Therapy.International journal of molecular sciences · 2019
    Review
  19. Article
  20. MiR-125a-5p promotes osteoclastogenesis by targeting TNFRSF1B.Cellular & molecular biology letters · 2019
    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

9 authors at 2 institutions in 1 country.

Yuval ZurDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Lior RosenfeldDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Chen Anna KeshelmanThe National Institute for Biotechnology in the Negev (NIBN), Beer-Sheva, Israel.
Nofar DalalDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Gali Guterman-RamDepartment of Physiology and Cell Biology, Regenerative Medicine and Stem Cell Research Center (RMSC), Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Ayelet OrenbuchDepartment of Physiology and Cell Biology, Regenerative Medicine and Stem Cell Research Center (RMSC), Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Yulia EinavFaculty of Engineering, Holon Institute of Technology, Holon, Israel.
Noam LevaotDepartment of Physiology and Cell Biology, Regenerative Medicine and Stem Cell Research Center (RMSC), Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Niv PapoDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel.ORCID 0000-0002-7056-2418
Ben-Gurion University of the Negev · ILHolon Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is currently a demand for new highly efficient and specific drugs to treat osteoporosis, a chronic bone disease affecting millions of people worldwide. We have developed a combinatorial strategy for engineering bispecific inhibitors that simultaneously target the unique combination of c-FMS and αvβ3 integrin, which act in concert to facilitate bone resorption by osteoclasts. Using functional fluorescence-activated cell sorting (FACS)-based screening assays of random mutagenesis macrophage colony-stimulating factor (M-CSF) libraries against c-FMS and αvβ3 integrin, we engineered dual-specific M-CSF mutants with high affinity to both receptors. These bispecific mutants act as functional antagonists of c-FMS and αvβ3 integrin activation and hence of osteoclast differentiation in vitro and osteoclast activity in vivo. This study thus introduces a versatile platform for the creation of new-generation therapeutics with high efficacy and specificity for osteoporosis and other bone diseases. It also provides new tools for studying molecular mechanisms and the cell signaling pathways that mediate osteoclast differentiation and function.

Indexed as

AnimalsBinding SitesBone Density Conservation AgentsBone Marrow CellsBone ResorptionCell DifferentiationCloning, MolecularEscherichia coliGene ExpressionGene Expression RegulationHumansIntegrin alphaVbeta3Macrophage Colony-Stimulating FactorMacrophagesMiceMolecular Docking SimulationBone Density Conservation AgentsIntegrin alphaVbeta3Macrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating FactorRecombinant Proteins

Identifiers

PMID30142160
PMCPMC6126843
OpenAlexW2888755470

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.