Evidence map›Paper›PMID 21081493›Full record

ArticleThe Journal of biological chemistry2011

PARP-14 functions as a transcriptional switch for Stat6-dependent gene activation.

Purvi Mehrotra, Jonathan P Riley, Ravi Patel, Fang Li, Le'erin Voss, Shreevrat Goenka

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

80 citing papers in PubMed, 144 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Butyrate, IL-4, and EP4 Receptors: A Triad of Colorectal Homeostasis, Protecting Against Onset of Cancer and IBD?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Body-wide genetic deficiency of poly(ADP-ribose) polymerase 14 sensitizes mice to colitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. [1,2,4]Triazolo[3,4-Journal of medicinal chemistry · 2023
    Article

20 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

6 authors at 2 institutions in 1 country.

Purvi MehrotraDepartment of Pediatrics, HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Jonathan P Riley
Ravi Patel
Fang Li
Le'erin Voss
Shreevrat Goenka
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

PARP activity in allergic inflammationR01HL093105 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPLAN, MARK H · 2009 to 2012
$1.5M
NHLBI NIH HHS HL093105NHLBI NIH HHS R01 HL093105
6 · The paper itself

Abstract

A subset of poly ADP-ribose polymerases (PARP) that also contain macro domains regulate transcription. One such macro PARP, PARP-14 alters interleukin 4 (IL-4) and Stat6-dependent transcription. Stat6, activated by IL-4 plays an important role in T helper cell immunity and B cell responses. Here we define the mechanism by which PARP-14 regulates Stat6-activated transcription. Under non-stimulating conditions, PARP-14 recruits HDAC 2 and 3 to IL-4 responsive promoters. In the presence of IL-4, PARP-14 promotes efficient binding of Stat6 to its target genes. Moreover, HDAC 2 and 3 are released from the promoter with an IL-4 signal, this is aided by the ADP-ribosylation of the HDACs by PARP-14. The HDACs and PARP-14 get replaced by coactivators containing HAT activity. Based on these observations we put forth a mechanism in which PARP-14 functions as a transcriptional switch for Stat6-dependent gene induction. Thus, in the absence of a signal PARP-14 acts as a transcriptional repressor by recruiting HDACs. In contrast, in the presence of IL-4 the catalytic activity of PARP-14 facilitates Stat6 binding to the promoter, and release of HDACs so as to activate transcription.

Indexed as

AnimalsCell LineHistone Deacetylase 2Histone Deacetylase 3Histone DeacetylasesInterleukin-4MiceMice, KnockoutPoly(ADP-ribose) PolymerasesPromoter Regions, GeneticRepressor ProteinsSTAT6 Transcription FactorT-Lymphocytes, Helper-InducerTranscription, GeneticHdac2 protein, mouseHistone Deacetylase 2Histone Deacetylase 3Histone DeacetylasesInterleukin-4Parp14 protein, mousePoly(ADP-ribose) PolymerasesRepressor ProteinsStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID21081493
PMCPMC3023471
OpenAlexW2096529411

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.