Evidence map›Paper›PMID 27884787›Full record

ArticleBone2017

Loss of Cbl-PI3K interaction modulates the periosteal response to fracture by enhancing osteogenic commitment and differentiation.

Vanessa Scanlon, Bhavita Walia, Jungeun Yu, Marc Hansen, Hicham Drissi, Peter Maye, Archana Sanjay

Open access · greenAbstract read
In one paragraph

Article in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  13. Tendon stem progenitor cells: Understanding the biology to inform therapeutic strategies for tendon repair.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. [Osteogenic effect of collagen/bioglass composites carrying noggin siRNA].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  18. Deubiquitinating Enzymes and Bone Remodeling.Stem cells international · 2018
    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

7 authors at 2 institutions in 1 country.

Vanessa ScanlonDepartment of Orthopaedic Surgery, United States.
Bhavita WaliaDepartment of Orthopaedic Surgery, United States; Department of Genetics and Genome Sciences, United States.
Jungeun YuDepartment of Orthopaedic Surgery, United States.
Marc HansenDepartment of Genetics and Genome Sciences, United States; Center for Molecular Medicine, United States.
Hicham DrissiDepartment of Orthopaedic Surgery, United States; Department of Genetics and Genome Sciences, United States.
Peter MayeDepartment of Reconstructive Sciences, UConn Health, Farmington, CT, United States.
Archana SanjayDepartment of Orthopaedic Surgery, United States; Department of Genetics and Genome Sciences, United States. Electronic address: asanjay@uchc.edu.
Human Genome Sciences (United States) · USUConn Health · US

Funding

Skeletal, Craniofacial and Oral Biology Training GrantT90DE021989 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MINA, MINA · 2011 to 2022
$4.5M
NIDCR NIH HHS T90 DE021989
6 · The paper itself

Abstract

The periosteum contains multipotent skeletal progenitors that contribute to bone repair. The signaling pathways regulating the response of periosteal cells to fracture are largely unknown. Phosphatidylinositol-3 Kinase (PI3K), a prominent lipid kinase, is a major signaling protein downstream of several factors that regulate osteoblast differentiation. Cbl is an E3 ubiquitin ligase and a major adaptor protein that binds to the p85 regulatory subunit and modulates PI3K activity. Substitution of tyrosine 737 to phenylalanine (Y737F) in Cbl abolishes the interaction between Cbl and p85 subunit without affecting the Cbl's ubiquitin ligase function. Here, we investigated the role of PI3K signaling during the very early stages of fracture healing using Osterix

Indexed as

Cell DifferentiationOsteogenesisAlkaline PhosphataseAnimalsBiomarkersCell CountCell LineageCell NucleusCell ProliferationFracture HealingFractures, BoneMesodermMice, Inbred C57BLMutationPeriosteumPhosphatidylinositol 3-KinaseAlkaline PhosphataseBiomarkersPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-cblSp7 protein, mouseSp7 Transcription FactorAlkaline Phosphatase activityFractureLaser capture microdissectionOsterixPeriosteumPI3K

Identifiers

PMID27884787
PMCPMC5819877
OpenAlexW2550883406

What OpenQuestion holds

Textmetadata
LicenceTDM
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.