Evidence map›Paper›PMID 21282370›Full record

ArticleDiabetes2011

Polymerase I and transcript release factor regulates lipolysis via a phosphorylation-dependent mechanism.

Nabila Aboulaich, Patricia C Chui, John M Asara, Jeffrey S Flier, Eleftheria Maratos-Flier

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Lessons from cavin-1 deficiency.Biochemical Society transactions · 2020
    Review
  3. Article
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  12. Review
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  14. Polymerase I and transcript release factor (PTRF) regulates adipocyte differentiation and determines adipose tissue expandability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  15. Review
  16. Pleiotropic effects of cavin-1 deficiency on lipid metabolism.The Journal of biological chemistry · 2014
    Article
  17. Article
  18. Review
  19. Review
  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

5 authors at 2 institutions in 1 country.

Nabila AboulaichDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Patricia C Chui
John M Asara
Jeffrey S Flier
Eleftheria Maratos-Flier
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

LEPTIN-- SIGNALING, TARGETS AND RESISTANCER37DK028082 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FLIER, JEFFREY S · 1992 to 2009
$5.7M
Actions of Melanin Concentrating Hormone in the BrainR01DK069983 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MARATOS-FLIER, ELEFTHERIA · 2006 to 2010
$1.6M
NIDDK NIH HHS R01 DK069983NIDDK NIH HHS R01-DK-069983NIDDK NIH HHS R37 DK028082NIDDK NIH HHS R37-DK-28082
6 · The paper itself

Abstract

objectivePolymerase I and transcript release factor (PTRF) is a protein highly expressed in adipose tissue and is an integral structural component of caveolae. Here, we report on a novel role of PTRF in lipid mobilization. RESEARCH DESIGN AND

methodsPTRF expression was examined in different adipose depots of mice during fasting, refeeding, and after administration of catecholamines and insulin. Involvement of PTRF during lipolysis was studied upon PTRF knockdown and overexpression and mutation of PTRF phosphorylation sites in 3T3-L1 adipocytes.

resultsPTRF expression in mouse white adipose tissue (WAT) is regulated by nutritional status, increasing during fasting and decreasing to baseline after refeeding. Expression of PTRF also is hormonally regulated because treatment of mice with insulin leads to a decrease in expression, whereas isoproterenol increases expression in WAT. Manipulation of PTRF levels revealed a role of PTRF in lipolysis. Lentiviral-mediated knockdown of PTRF resulted in a marked attenuation of glycerol release in response to isoproterenol. Conversely, overexpressing PTRF enhanced isoproterenol-stimulated glycerol release. Mass-spectrometric analysis revealed that PTRF is phosphorylated at multiple sites in WAT. Mutation of serine 42, threonine 304, or serine 368 to alanine reduced isoproterenol-stimulated glycerol release in 3T3-L1 adipocytes.

conclusionsOur study is the first direct demonstration for a novel adipose tissue-specific function of PTRF as a mediator of lipolysis and also shows that phosphorylation of PTRF is required for efficient fat mobilization.

Indexed as

3T3 CellsAdipocytesAdipose TissueAdrenergic beta-AgonistsAnimalsBlotting, WesternCells, CulturedChromatography, LiquidInsulinIsoproterenolLipolysisMembrane ProteinsMiceOrgan SpecificityPhosphorylationReverse Transcriptase Polymerase Chain ReactionAdrenergic beta-AgonistsCavin1 protein, mouseInsulinIsoproterenolMembrane ProteinsRNA-Binding ProteinsRNA, MessengerRNA, Small Interfering

Identifiers

PMID21282370
PMCPMC3046836
OpenAlexW2158150118

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.