Evidence map›Paper›PMID 25368164›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

c-Abl tyrosine kinase promotes adipocyte differentiation by targeting PPAR-gamma 2.

Rom Keshet, Zina Bryansker Kraitshtein, Matan Shanzer, Julia Adler, Nina Reuven, Yosef Shaul

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. GαMetabolites · 2026
    Article
  3. Article
  4. RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
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  8. Regulation of PPARγ2 Stability and Activity by SHP-1.Molecular and cellular biology · 2024
    Article
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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

6 authors at 1 institution in 1 country.

Rom KeshetDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Zina Bryansker KraitshteinDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Matan ShanzerDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Julia AdlerDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Nina ReuvenDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
Yosef ShaulDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel yosef.shaul@weizmann.ac.il.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipocyte differentiation, or adipogenesis, is a complex and highly regulated process. A recent proteomic analysis has predicted that the nonreceptor tyrosine kinase Abelson murine leukemia viral oncogene (c-Abl) is a putative key regulator of adipogenesis, but the underlying mechanism remained obscure. We found that c-Abl was activated during the early phase of mouse 3T3-L1 preadipocyte differentiation. Moreover, c-Abl activity was essential and its inhibition blocked differentiation to mature adipocytes. c-Abl directly controlled the expression and activity of the master adipogenic regulator peroxisome proliferator-activator receptor gamma 2 (PPARγ2). PPARγ2 physically associated with c-Abl and underwent phosphorylation on two tyrosine residues within its regulatory activation function 1 (AF1) domain. We demonstrated that this process positively regulates PPARγ2 stability and adipogenesis. Remarkably, c-Abl binding to PPARγ2 required the Pro12 residue that has a phenotypically well-studied common human genetic proline 12 alanine substitution (Pro12Ala) polymorphism. Our findings establish a critical role for c-Abl in adipocyte differentiation and explain the behavior of the known Pro12Ala polymorphism.

Indexed as

3T3-L1 CellsAdipocytesAdipogenesisAnimalsBenzamidesHEK293 CellsHumansImatinib MesylateMiceMutation, MissenseNIH 3T3 CellsPhosphorylationPhosphotyrosinePiperazinesPoint MutationPolymorphism, Single NucleotideBenzamidesImatinib MesylatePhosphotyrosinePiperazinesPPAR gammaProlineProtein IsoformsProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrimidinesadipogenesisc-AbldifferentiationPPAR gammaPro12Ala polymorphism

Identifiers

PMID25368164
PMCPMC4246298
OpenAlexW2107672532

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.