Evidence map›Paper›PMID 35737830›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Loss of adipose TET proteins enhances β-adrenergic responses and protects against obesity by epigenetic regulation of β3-AR expression.

Seongjun Byun, Chan Hyeong Lee, Hyeongmin Jeong, Hyejin Kim, Hyug Moo Kwon, Sungho Park, Kyungjae Myung, Jungeun An, Myunggon Ko

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  9. TET3-overexpressing macrophages promote endometriosis.The Journal of clinical investigation · 2024
    Article
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  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. The regulation of adipocyte growth in white adipose tissue.Frontiers in cell and developmental biology · 2022
    Review
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 1 institution in 2 countries.

Seongjun ByunDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Chan Hyeong LeeDepartment of Life Sciences, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Hyeongmin JeongDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Hyejin KimDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Hyug Moo KwonDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Sungho ParkDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Kyungjae MyungDepartment of Biomedical Engineering, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.ORCID 0000-0001-7975-6190
Jungeun AnDepartment of Life Sciences, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Myunggon KoDepartment of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
Harvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-adrenergic receptor (β-AR) signaling plays predominant roles in modulating energy expenditure by triggering lipolysis and thermogenesis in adipose tissue, thereby conferring obesity resistance. Obesity is associated with diminished β3-adrenergic receptor (β3-AR) expression and decreased β-adrenergic responses, but the molecular mechanism coupling nutrient overload to catecholamine resistance remains poorly defined. Ten-eleven translocation (TET) proteins are dioxygenases that alter the methylation status of DNA by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine and further oxidized derivatives. Here, we show that TET proteins are pivotal epigenetic suppressors of β3-AR expression in adipocytes, thereby attenuating the responsiveness to β-adrenergic stimulation. Deletion of all three

Indexed as

Epigenesis, GeneticGene Expression RegulationProto-Oncogene ProteinsAdipose Tissue, BrownAnimalsMiceObesityReceptors, Adrenergic, betaReceptors, Adrenergic, beta-3ThermogenesisProto-Oncogene ProteinsReceptors, Adrenergic, betaReceptors, Adrenergic, beta-3catecholamine resistanceHDACsobesityTET proteinsβ3-AR

Identifiers

PMID35737830
PMCPMC9245707
OpenAlexW4283313066

What Socratic 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 Socratic graph.