Evidence map›Paper›PMID 28180926›Full record

ArticleCellular and molecular life sciences : CMLS2017

WIP1 phosphatase is a critical regulator of adipogenesis through dephosphorylating PPARγ serine 112.

Dahu Li, Lijun Zhang, Lun Xu, Lili Liu, Yunling He, Yiyao Zhang, Xin Huang, Tong Zhao, Liying Wu, Yongqi Zhao and 7 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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  10. Article
  11. Functional Regulation of PPARs through Post-Translational Modifications.International journal of molecular sciences · 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

17 authors at 3 institutions in 1 country.

Dahu LiDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Lijun ZhangDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Lun XuDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Lili LiuDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Yunling HeDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Yiyao ZhangDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Xin HuangDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Tong ZhaoDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Liying WuDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Yongqi ZhaoDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Kuiwu WuDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Hui LiDepartment of Physiology, School of Medicine, Shandong University, Jinan, 250012, China.
Xiao YuDepartment of Physiology, School of Medicine, Shandong University, Jinan, 250012, China.
Taiyun ZhaoBeijing Institute of Pharmacology and Toxicology, Beijing, 100850, China.
Shenghui GongDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
Ming FanDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China. fanming@nic.bmi.ac.cn.
Lingling ZhuDepartment of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China. linglingzhu@hotmail.com.
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesNantong University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

WIP1, as a critical phosphatase, plays many important roles in various physiological and pathological processes through dephosphorylating different substrate proteins. However, the functions of WIP1 in adipogenesis and fat accumulation are not clear. Here, we report that WIP1-deficient mice show impaired body weight growth, dramatically decreased fat mass, and significantly reduced triglyceride and leptin levels in circulation. This dysregulation of adipose development caused by the deletion of WIP1 occurs as early as adipogenesis. In contrast, lentivirus-mediated WIP1 phosphatase overexpression significantly increases the adipogenesis of pre-adipocytes via an enzymatic activity-dependent mechanism. PPARγ is a master gene of adipogenesis, and the phosphorylation of PPARγ at serine 112 strongly inhibits adipogenesis; however, very little is known about the negative regulation of this phosphorylation. Here, we show that WIP1 phosphatase plays a pro-adipogenic role by interacting directly with PPARγ and dephosphorylating p-PPARγ S112 in vitro and in vivo.

Indexed as

AdipogenesisAdipocytesAdiposityAnimalsBody WeightCell LineCell SizeGene Expression RegulationGene Knockdown TechniquesHumansLeptinMice, Inbred C57BLMice, KnockoutPhosphorylationPhosphoserinePPAR gammaLeptinPhosphoserinePPAR gammaPpm1d protein, mouseProtein Phosphatase 2CTriglyceridesAdipogenesisAdiposityDephosphorylationPPARγWIP1 phosphatase

Identifiers

PMID28180926
PMCPMC11107755
OpenAlexW2586913959

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.