Evidence map›Paper›PMID 28287536›Full record

ArticleJournal of visualized experiments : JoVE2017

Stimulation of Notch Signaling in Mouse Osteoclast Precursors.

Gurpreet Kaur, Jaimo Ahn, Kurt D Hankenson, Jason W Ashley

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Journal of visualized experiments : JoVE, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Suppression of Notch Signaling in Osteoclasts Improves Bone Regeneration and Healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019
    Article
  4. Notch signaling inhibition protects against LPS mediated osteolysis.Biochemical and biophysical research communications · 2019
    Article
  5. Review
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 2 institutions in 1 country.

Gurpreet KaurDepartment of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania; Department of Biological Sciences, University of the Sciences.
Jaimo AhnDepartment of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania.
Kurt D HankensonDepartment of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania; The Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University.
Jason W AshleyDepartment of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania; Department of Biology, College of Science, Technology, Engineering, & Mathematics, Eastern Washington University; jashley6@ewu.edu.
University of Pennsylvania · USEastern Washington University · US

Funding

University of Pennsylvania Postdoctoral Opportunities in Research and TeachingK12GM081259 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI Janis K. Burkhardt · 2007 to 2026
$20.1M
The Role of Hyaluronic Acid Receptors in Tendon HealingP30AR050950 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI SOSLOWSKY, LOUIS J · 2006 to 2015
$6.2M
NIAMS NIH HHS P30 AR050950NIGMS NIH HHS K12 GM081259
6 · The paper itself

Abstract

Notch signaling is a key component of multiple physiological and pathological processes. The nature of Notch signaling, however, makes in vitro investigation of its varying and sometimes contradictory roles a challenge. As a component of direct cell-cell communication with both receptors and ligands bound to the plasma membrane, Notch signaling cannot be activated in vitro by simple addition of ligands to culture media, as is possible with many other signaling pathways. Instead, Notch ligands must be presented to cells in an immobilized state. Variations in methods of Notch signaling activation can lead to different outcomes in cultured cells. In osteoclast precursors, in particular, differences in methods of Notch stimulation and osteoclast precursor culture and differentiation have led to disagreement over whether Notch signaling is a positive or negative regulator of osteoclast differentiation. While closer comparisons of osteoclast differentiation under different Notch stimulation conditions in vitro and genetic models have largely resolved the controversy regarding Notch signaling and osteoclasts, standardized methods of continuous and temporary stimulation of Notch signaling in cultured cells could prevent such discrepancies in the future. This protocol describes two methods for stimulating Notch signaling specifically in cultured mouse osteoclast precursors, though these methods should be applicable to any adherent cell type with minor adjustments. The first method produces continuous stimulation of Notch signaling and involves immobilizing Notch ligand to a tissue culture surface prior to the seeding of cells. The second, which uses Notch ligand bound to agarose beads allows for temporary stimulation of Notch signaling in cells that are already adhered to a culture surface. This protocol also includes methods for detecting Notch activation in osteoclast precursors as well as representative transcriptional markers of Notch signaling activation.

Indexed as

AnimalsCarrier ProteinsCell DifferentiationCells, CulturedMiceModels, AnimalOsteoclastsReceptors, NotchSignal TransductionCarrier ProteinsReceptors, Notch

Identifiers

PMID28287536
PMCPMC5408895
OpenAlexW2592034610

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.