Evidence map›Paper›PMID 28107648›Full record

ArticleMolecular cell2017

PARP-1 Controls the Adipogenic Transcriptional Program by PARylating C/EBPβ and Modulating Its Transcriptional Activity.

Xin Luo, Keun Woo Ryu, Dae-Seok Kim, Tulip Nandu, Carlos J Medina, Rebecca Gupte, Bryan A Gibson, Raymond E Soccio, Yonghao Yu, Rana K Gupta and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. SOCS3 Stabilizes PARP1 to Suppress Adipogenic Transcription and Abdominal Adipogenesis in Avian.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. NADCell reports · 2026
    Article
  4. SRY mediates male-specific susceptibility to acute liver injury.Cell communication and signaling : CCS · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Regulation of adipogenesis by nucleotides.Biochemical Society transactions · 2025
    Review
  9. Article
  10. Prospects for PARG inhibitors in cancer therapy.Journal of molecular cell biology · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

17 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

11 authors at 2 institutions in 1 country.

Xin LuoLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Program in Genetics, Development, and Disease, Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Keun Woo RyuLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Program in Genetics, Development, and Disease, Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Dae-Seok KimLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Tulip NanduLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Carlos J MedinaDivision of Endocrinology, Diabetes, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Rebecca GupteLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Bryan A GibsonLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Program in Molecular Biophysics, Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Raymond E SoccioDivision of Endocrinology, Diabetes, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Yonghao YuDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Rana K GuptaDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
W Lee KrausLaboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Basic Research, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Program in Genetics, Development, and Disease, Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: lee.kraus@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USUniversity of Pennsylvania · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MELANIE H. COBB · 2010 to 2026
$53.7M
Dose-Dependent Effects of Hormone on the Activity of Estrogen Receptor Enhancers and Target GenesR01DK058110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAM Lee KRAUS · 2000 to 2026
$10.4M
The Role of PARP-1 in Hormone-Regulated TranscriptionR01DK069710 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI KRAUS, WILLIAM LEE · 2004 to 2025
$7.9M
Establishment and Maintenance of Healthy Adipose Tissue in ObesityR01DK104789 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GUPTA, RANA K · 2015 to 2024
$3.9M
Translating human PPARy binding regions to gene regulation and metabolic diseaseK08DK094968 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SOCCIO, RAYMOND EDWARD · 2012 to 2016
$775k
NCI NIH HHS P30 CA142543NIDDK NIH HHS K08 DK094968NIDDK NIH HHS R01 DK058110NIDDK NIH HHS R01 DK069710NIDDK NIH HHS R01 DK104789
6 · The paper itself

Abstract

Poly(ADP-ribosyl)ation (PARylation) is a post-translational modification of proteins mediated by PARP family members, such as PARP-1. Although PARylation has been studied extensively, few examples of definitive biological roles for site-specific PARylation have been reported. Here we show that C/EBPβ, a key pro-adipogenic transcription factor, is PARylated by PARP-1 on three amino acids in a conserved regulatory domain. PARylation at these sites inhibits C/EBPβ's DNA binding and transcriptional activities and attenuates adipogenesis in various genetic and cell-based models. Interestingly, PARP-1 catalytic activity drops precipitously during the first 48 hr of differentiation, corresponding to a release of C/EBPβ from PARylation-mediated inhibition. This promotes the binding of C/EBPβ at enhancers controlling the expression of adipogenic target genes and continued differentiation. Depletion or chemical inhibition of PARP-1, or mutation of the PARylation sites on C/EBPβ, enhances these early adipogenic events. Collectively, our results provide a clear example of how site-specific PARylation drives biological outcomes.

Indexed as

AdipogenesisProtein Processing, Post-TranslationalTranscription, Genetic3T3-L1 CellsAdipocytesAnimalsBinding SitesCCAAT-Enhancer-Binding Protein-betaDNAEmbryonic Stem CellsGenotypeMaleMiceMice, Inbred C57BLMice, KnockoutMutationCCAAT-Enhancer-Binding Protein-betaCebpb protein, mouseDNAParp1 protein, mousePoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsadipogenesisC/EBPβDNA bindinggene expressionPARP-1PARP inhibitorPARylationpoly(ADP-ribose)transcription

Identifiers

PMID28107648
PMCPMC5258183
OpenAlexW2577827693

What OpenQuestion holds

Textmetadata
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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.