Evidence map›Paper›PMID 21913895›Full record

ArticleBritish journal of pharmacology2012

TM-25659 enhances osteogenic differentiation and suppresses adipogenic differentiation by modulating the transcriptional co-activator TAZ.

E J Jang, H Jeong, J O Kang, N J Kim, M S Kim, S H Choi, S E Yoo, J H Hong, M A Bae, E S Hwang

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. MOB1 deletion in murine mature adipocytes ameliorates obesity and diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
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  5. Article
  6. Review
  7. TAZ promotes PDX1-mediated insulinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Article
  8. The essential role of TAZ in normal tissue homeostasis.Archives of pharmacal research · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The role of microRNAs in bone remodeling.International journal of oral science · 2015
    Review
  20. 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

10 authors at 3 institutions in 1 country.

E J JangCollege of Pharmacy and Division of Life and Pharmaceutical Sciences and Center for Cell Signaling and Drug Discovery Research, Ewha Womans University, Seoul Korea.
H Jeong
J O Kang
N J Kim
M S Kim
S H Choi
S E Yoo
J H Hong
M A Bae
E S Hwang
Korea Research Institute of Chemical Technology · KREwha Womans University · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe transcriptional co-activator with PDZ-binding motif (TAZ) is characterized as a transcriptional modulator of mesenchymal stem cell differentiation into osteoblasts and adipocytes. Moreover, increased TAZ activity in the nucleus enhances osteoblast differentiation and suppresses adipocyte development by interacting with runt-related transcription factor 2 (RUNX2) and PPARγ, respectively. Therefore, it would be of interest to identify low MW compounds that modulate nuclear TAZ activity. EXPERIMENTAL APPROACH: High-throughput screening was performed using a library of low MW compounds in order to identify TAZ modulators that enhance nuclear TAZ localization. The effects and molecular mechanisms of a TAZ modulator have been characterized in osteoblast and adipocyte differentiation. KEY

resultsWe identified 2-butyl-5-methyl-6-(pyridine-3-yl)-3-[2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl]-3H-imidazo[4,5-b]pyridine] (TM-25659) as a TAZ modulator. TM-25659 enhanced nuclear TAZ localization in a dose-dependent manner and attenuated PPARγ-mediated adipocyte differentiation by facilitating PPARγ suppression activity of TAZ. In addition, TAZ-induced RUNX2 activity activation was further increased in osteoblasts, causing increased osteoblast differentiation. Accordingly, TM-25659 suppressed bone loss in vivo and decreased weight gain in an obesity model. After oral administration, TM-25659 had a favourable pharmacokinetic profile. CONCLUSION AND IMPLICATIONS: TM-25659 stimulated nuclear TAZ localization and thus caused TAZ to suppress PPARγ-dependent adipogenesis and enhance RUNX2-induced osteoblast differentiation in vitro and in vivo. Our data suggest that TM-25659 could be beneficial in the control of obesity and bone loss.

Indexed as

3T3-L1 CellsAdaptor Proteins, Signal TransducingAdipocytesAdipogenesisAnimalsBone ResorptionBridged Bicyclo Compounds, HeterocyclicCell DifferentiationCell NucleusCells, CulturedChlorocebus aethiopsCore Binding Factor Alpha 1 SubunitCOS CellsHEK293 CellsHumansMale2-butyl-5-methyl-6-(pyridine-3-yl)-3-(2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl)-3H-imidazo(4,5-b)pyridineAdaptor Proteins, Signal TransducingBridged Bicyclo Compounds, HeterocyclicCore Binding Factor Alpha 1 SubunitPPAR gammaSmall Molecule LibrariesTetrazolesTrans-ActivatorsWwtr1 protein, mouse

Identifiers

PMID21913895
PMCPMC3372739
OpenAlexW1656842517

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.