Evidence map›Paper›PMID 33850312›Full record

ArticleCellular & molecular immunology2021

Ssu72 is a T-cell receptor-responsive modifier that is indispensable for regulatory T cells.

Jin-Kwan Lee, Seo-Young Koo, Hye-Mi Nam, Jee-Boong Lee, Jiwon Ko, Kyung-Mo Kim, Eun-Ji Park, Tae Jin Kim, Ho Lee, Heounjeong Go and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Ssu72 Dual-Specific Protein Phosphatase: From Gene to Diseases.International journal of molecular sciences · 2021
    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

11 authors at 5 institutions in 2 countries.

Jin-Kwan Lee *Research Institute, Curogen Technology, Suwon, South Korea.ORCID http://orcid.org/0000-0002-7068-7165
Seo-Young Koo *Department of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
Hye-Mi NamDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
Jee-Boong LeeDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
Jiwon KoDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
Kyung-Mo KimDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
Eun-Ji ParkDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
Tae Jin KimDepartment of Immunology, Sungkyunkwan University School of Medicine, Seoul, South Korea.ORCID http://orcid.org/0000-0001-9802-0568
Ho LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, Research Institute, National Cancer Center, Gyeonggi, South Korea. ho25lee@ncc.re.kr.
Heounjeong GoAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. damul37@amc.seoul.kr.
Chang-Woo LeeResearch Institute, Curogen Technology, Suwon, South Korea. cwlee1234@skku.edu.
Samsung Medical Center · KRUlsan College · KRNational Cancer Center · USSK Group (South Korea) · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The homeostatic balance between effector T cells and regulatory T cells (Tregs) is crucial for adaptive immunity; however, epigenetic programs that inhibit phosphorylation to regulate Treg development, peripheral expression, and suppressive activity are elusive. Here, we found that the Ssu72 phosphatase is activated by various T-cell receptor signaling pathways, including the T-cell receptor and IL-2R pathways, and localizes at the cell membrane. Deletion of Ssu72 in T cells disrupts CD4

Indexed as

Cell DifferentiationHomeostasisSignal TransductionAnimalsCell LineageDisease SusceptibilityForkhead Transcription FactorsImmune ToleranceInflammatory Bowel DiseasesMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalNuclear Receptor Subfamily 1, Group F, Member 3Phospholipase C gammaPhosphoprotein PhosphatasesForkhead Transcription FactorsFoxp3 protein, mouseNuclear Receptor Subfamily 1, Group F, Member 3Phospholipase C gammaPhosphoprotein PhosphatasesReceptors, Antigen, T-CellRorc protein, mousessu72 protein, mouseAutoimmunityFoxP3Regulatory T cellsSsu72T cell receptor

Identifiers

PMID33850312
PMCPMC8166877
OpenAlexW3156837440

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.