Evidence map›Paper›PMID 31003455›Full record

ArticleCancers2019

Complementary Roles of GCN5 and PCAF in Foxp3+ T-Regulatory Cells.

Yujie Liu, Chunrong Bao, Liqing Wang, Rongxiang Han, Ulf H Beier, Tatiana Akimova, Philip A Cole, Sharon Y R Dent, Wayne W Hancock

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. Protein acetylation: a novel modus of obesity regulation.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021
    Review
  13. Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021
    Review
  14. 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

9 authors at 3 institutions in 1 country.

Yujie LiuTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. yujieliu2010@gmail.com.
Chunrong BaoTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. bcron@126.com.
Liqing WangTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. wangl@email.chop.edu.
Rongxiang HanTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. hanr@email.chop.edu.
Ulf H BeierDivision of Nephrology, Department of Pediatrics, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. beieru@email.chop.edu.
Tatiana AkimovaTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Tatiana.Akimova@pennmedicine.upenn.edu.
Philip A ColeDepartment of Biological Chemistry and Molecular Pharmacology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. pacole@bwh.harvard.edu.
Sharon Y R DentDepartment of Epigenetics and Molecular Carcinogenesis, Center for Cancer Epigenetics, University of Texas MD Anderson Cancer Center Science Park, Smithville, TX 78957, USA. sroth@mdanderson.org.ORCID 0000-0002-4824-3269
Wayne W HancockTransplant Immunology, Department of Pathology & Laboratory Medicine & Biesecker Center for Study of Pediatric Liver Diseases, Children's Hospital of Philadelphia, and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. whancock@pennmedicine.upenn.edu.ORCID 0000-0002-7211-5291
Children's Hospital of Philadelphia · USBrigham and Women's Hospital · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Protein Acylation and Methylation Mechanisms_Administrative SupplementR37GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2013 to 2022
$4.1M
NCI NIH HHS P30 CA016672NIGMS NIH HHS R37 GM062437NIH HHS CA158941, AI123241, AI095353 and GM62437
6 · The paper itself

Abstract

Functions of the GCN5-related N-acetyltransferase (GNAT) family of histone/protein acetyltransferases (HATs) in Foxp3+ T-regulatory (Treg) cells are unexplored, despite the general importance of these enzymes in cell biology. We now show that two prototypical GNAT family members, GCN5 (general control nonrepressed-protein 5, lysine acetyltransferase (KAT)2a) and p300/CBP-associated factor (p300/CBP-associated factor (PCAF), Kat2b) contribute to Treg functions through partially distinct and partially overlapping mechanisms. Deletion of Gcn5 or PCAF did not affect Treg development or suppressive function in vitro, but did affect inducible Treg (iTreg) development, and in vivo, abrogated Treg-dependent allograft survival. Contrasting effects were seen upon targeting of each HAT in all T cells; mice lacking GCN5 showed prolonged allograft survival, suggesting this HAT might be a target for epigenetic therapy in allograft recipients, whereas transplants in mice lacking PCAF underwent acute allograft rejection. PCAF deletion also enhanced anti-tumor immunity in immunocompetent mice. Dual deletion of GCN5 and PCAF led to decreased Treg stability and numbers in peripheral lymphoid tissues, and mice succumbed to severe autoimmunity by 3-4 weeks of life. These data indicate that HATs of the GNAT family have contributions to Treg function that cannot be replaced by the functions of previously characterized Treg HATs (CBP, p300, and Tip60), and may be useful targets in immuno-oncology.

Indexed as

acetylationacetyltransferaseanti-tumor immunityautoimmunitychromatinepigeneticstransplantationTreg cells

Identifiers

PMID31003455
PMCPMC6520961
OpenAlexW2939476688

What OpenQuestion holds

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LicenceCC BY
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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.