Evidence map›Paper›PMID 32807497›Full record

ArticleBiochemical and biophysical research communications2020

TAOK3 is a MAP3K contributing to osteoblast differentiation and skeletal mineralization.

Zan Li, Hwanhee Oh, Michelle Cung, Sofia Jenia Marquez, Jun Sun, Hamida Hammad, Sophie Janssens, Philippe Pouliot, Bart N Lambrecht, Yeon-Suk Yang and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  7. Review
  8. Article
  9. Genome-wide Mendelian randomization identifies actionable novel drug targets for psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. The Diverse Roles of TAO Kinases in Health and Diseases.International journal of molecular sciences · 2020
    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

12 authors at 5 institutions in 4 countries.

Zan LiDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA; Department of Sports Medicine & Research Center of Sports Medicine, Xiangya Hospital, Central South University, Changsha, 410008, People's Republic of China.
Hwanhee OhDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA.
Michelle CungDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA.
Sofia Jenia MarquezDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA.
Jun SunDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA.
Hamida HammadVIB Inflammation Research Center, Department of Respiratory Medicine, Ghent University, Ghent, Belgium; Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
Sophie JanssensVIB Inflammation Research Center, Department of Respiratory Medicine, Ghent University, Ghent, Belgium; Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
Philippe PouliotVIB Inflammation Research Center, Department of Respiratory Medicine, Ghent University, Ghent, Belgium.
Bart N LambrechtVIB Inflammation Research Center, Department of Respiratory Medicine, Ghent University, Ghent, Belgium; Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
Yeon-Suk YangDivision of Rheumatology, Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA01605, USA.
Jae-Hyuck ShimDivision of Rheumatology, Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA01605, USA. Electronic address: jaehyuck.shim@umassmed.edu.
Matthew B GreenblattDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, USA. Electronic address: mag3003@med.cornell.edu.
Cornell University · USErasmus MC · NLUniversity of Massachusetts Chan Medical School · USCentral South University · CNGhent University · BE

Funding

Modulation of Bone Formation by SHN3DP5OD021351 · OD · WEILL MEDICAL COLL OF CORNELL UNIV · PI GREENBLATT, MATTHEW BLAKE · 2015 to 2019
$2.1M
Identification of novel regulators governing osteoclast-osteoblast couplingR01AR068983 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI SHIM, JAE-HYUCK · 2016 to 2020
$1.9M
"Establishing Pathways for Endothelial Support of Bone Formation with SLIT3"R01AR075585 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI GREENBLATT, MATTHEW BLAKE · 2020 to 2024
$1.8M
Novel approach to promote bone formation in osteoporosis using bone-homing mesenchymal stem cellsR21AR073331 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI SHIM, JAE-HYUCK, TUNG, CHING-HSUAN · 2018 to 2019
$425k
A novel bone-targeting AAV-mediated gene therapy to promote bone formation in osteoporosisR21AR077557 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHIM, JAE-HYUCK · 2021 to 2022
$403k
NIAMS NIH HHS R01 AR068983NIAMS NIH HHS R01 AR075585NIAMS NIH HHS R21 AR073331NIAMS NIH HHS R21 AR077557NIH HHS DP5 OD021351
6 · The paper itself

Abstract

Current anabolic drugs to treat osteoporosis and other disorders of low bone mass all have important limitations in terms of toxicity, contraindications, or poor efficacy in certain contexts. Addressing these limitations will require a better understanding of the molecular pathways, such as the mitogen activated protein kinase (MAPK) pathways, that govern osteoblast differentiation and, thereby, skeletal mineralization. Whereas MAP3Ks functioning in the extracellular signal-regulated kinases (ERK) and p38 pathways have been identified in osteoblasts, MAP3Ks mediating proximal activation of the c-Jun N-terminal kinase (JNK) pathway have yet to be identified. Here, we demonstrate that thousand-and-one kinase 3 (TAOK3, MAP3K18) functions as an upstream activator of the JNK pathway in osteoblasts both in vitro and in vivo. Taok3-deficient osteoblasts displayed defective JNK pathway activation and a marked decrease in osteoblast differentiation markers and defective mineralization, which was also confirmed using TAOK3 deficient osteoblasts derived from human MSCs. Additionally, reduced expression of Taok3 in a murine model resulted in osteopenia that phenocopies aspects of the Jnk1-associated skeletal phenotype such as occipital hypomineralization. Thus, in vitro and in vivo evidence supports TAOK3 as a proximal activator of the JNK pathway in osteoblasts that plays a critical role in skeletal mineralization.

Indexed as

Cell DifferentiationAnimalsCalcification, PhysiologicCells, CulturedFemurGene ExpressionMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMice, Inbred C57BLMice, Mutant StrainsMitogen-Activated Protein Kinase 8OsteoblastsPhenotypeProtein Serine-Threonine KinasesX-Ray MicrotomographyMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 8Protein Serine-Threonine KinasesTAOK3 protein, humanBoneJNKMAPKOsteoblastsTAOK3

Identifiers

PMID32807497
PMCPMC7494564
OpenAlexW3049276537

What OpenQuestion holds

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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.