Evidence map›Paper›PMID 23236157›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Nonreceptor tyrosine phosphatase Shp2 promotes adipogenesis through inhibition of p38 MAP kinase.

Zhao He, Helen H Zhu, Timothy J Bauler, Jing Wang, Theodore Ciaraldi, Nazilla Alderson, Shuangwei Li, Marie-Astrid Raquil, Kaihong Ji, Shufen Wang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  5. A PolydnavirusViruses · 2022
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  17. The Opposite Expected Effect of p38 Inhibitors on Fat Graft Survival.Plastic and reconstructive surgery. Global open · 2016
    Article
  18. Review
  19. Article
  20. Article
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

14 authors at 3 institutions in 1 country.

Zhao HeDepartment of Pathology and Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093-0864, USA.
Helen H Zhu
Timothy J Bauler
Jing Wang
Theodore Ciaraldi
Nazilla Alderson
Shuangwei Li
Marie-Astrid Raquil
Kaihong Ji
Shufen Wang
Jianhua Shao
Robert R Henry
Philip D King
Gen-Sheng Feng
University of California, San Diego · USUniversity of Michigan–Ann Arbor · USVA San Diego Healthcare System · US

Funding

Coordinated regulation of signaling events for insulin biosynthesis and secretionR01DK075916 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FENG, GEN-SHENG · 2009 to 2013
$1.8M
Regulation of Leptin SignalingR01DK073945 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FENG, GEN-SHENG · 2007 to 2010
$1.5M
NIDDK NIH HHS DK075916NIDDK NIH HHS R01 DK073945NIDDK NIH HHS R01DK073945NIDDK NIH HHS R01 DK075916
6 · The paper itself

Abstract

The molecular mechanism underlying adipogenesis and the physiological functions of adipose tissue are not fully understood. We describe here a unique mouse model of severe lipodystrophy. Ablation of Ptpn11/Shp2 in adipocytes, mediated by aP2-Cre, led to premature death, lack of white fat, low blood pressure, compensatory erythrocytosis, and hepatic steatosis in Shp2(fat-/-) mice. Fat transplantation partially rescued the lifespan and blood pressure in Shp2(fat-/-) mice, and administration of leptin also restored partially the blood pressure of mutant animals with endogenous leptin deficiency. Consistently, homozygous deletion of Shp2 inhibited adipocyte differentiation from embryonic stem (ES) cells. Biochemical analyses suggest a Shp2-TAO2-p38-p300-PPARγ pathway in adipogenesis, in which Shp2 suppresses p38 activation, leading to stabilization of p300 and enhanced PPARγ expression. Inhibition of p38 restored adipocyte differentiation from Shp2(-/-) ES cells, and p38 signaling is also suppressed in obese patients and obese animals. These results illustrate an essential role of adipose tissue in mammalian survival and physiology and also suggest a common signaling mechanism involved in adipogenesis and obesity development.

Indexed as

Disease Models, AnimalAdipogenesisAdipose TissueAnimalsBlood PressureDNA PrimersE1A-Associated p300 ProteinGene DeletionLeptinLipodystrophyMiceMice, Knockoutp38 Mitogen-Activated Protein KinasesPPAR gammaProtein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 11DNA PrimersE1A-Associated p300 ProteinEp300 protein, mouseLeptinp38 Mitogen-Activated Protein KinasesPPAR gammaProtein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 11TAOK2 protein, human

Identifiers

PMID23236157
PMCPMC3538237
OpenAlexW2061638705

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.