Evidence map›Paper›PMID 24703692›Full record

ArticleCell metabolism2014

Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice.

Matthew J Harms, Jeff Ishibashi, Wenshan Wang, Hee-Woong Lim, Susumu Goyama, Tomohiko Sato, Mineo Kurokawa, Kyoung-Jae Won, Patrick Seale

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 1 pooled it
16.7field-weighted citation impact, top 1% 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

234 citing papers in PubMed, 1 synthesis or guideline pooled it, 383 citations in OpenAlex.

  1. Pooled it
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  7. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
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174 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Matthew J HarmsInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Jeff IshibashiInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Wenshan WangInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Hee-Woong LimInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Susumu GoyamaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Tomohiko SatoDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Mineo KurokawaDepartment of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Kyoung-Jae WonInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Patrick SealeInstitute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA. Electronic address: sealep@upenn.edu.
Translational Therapeutics (United States) · USThe University of Tokyo · JP

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Patrick Seale · 1986 to 2026
$48.3M
Molecular Regulation of Brown Adipose Cell Fate in Somitic Stem CellsDP2OD007288 · OD · UNIVERSITY OF PENNSYLVANIA · PI SEALE, PATRICK · 2010 to 2010
$2.4M
NIDDK NIH HHS DK19525NIDDK NIH HHS P30 DK019525NIH HHS DP2 OD007288NIH HHS DP2OD007288
6 · The paper itself

Abstract

Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. However, Prdm16 was required in young mice to suppress the expression of white-fat-selective genes in BAT through recruitment of the histone methyltransferase Ehmt1. Additionally, Prdm16 deficiency caused a severe adult-onset decline in the thermogenic character of interscapular BAT. This resulted in BAT dysfunction and cold sensitivity but did not predispose the animals to obesity. Interestingly, the loss of brown fat identity due to ablation of Prdm16 was accelerated by concurrent deletion of the closely related Prdm3 gene. Together, these results show that Prdm16 and Prdm3 control postnatal BAT identity and function.

Indexed as

Adipocytes, BrownAgingAnalysis of VarianceAnimalsBlotting, WesternChromatin ImmunoprecipitationDNA-Binding ProteinsFlow CytometryGene Expression Regulation, DevelopmentalHistological TechniquesHistone-Lysine N-MethyltransferaseMiceMice, KnockoutMicroarray AnalysisReal-Time Polymerase Chain ReactionTranscription FactorsDNA-Binding ProteinsGLP protein, mouseHistone-Lysine N-MethyltransferasePrdm16 protein, mouseTranscription Factors

Identifiers

PMID24703692
PMCPMC4012340
OpenAlexW2093743108

What OpenQuestion holds

Textmetadata
LicenceTDM
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.