Evidence map›Paper›PMID 26843327›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Yin Yang 1 Promotes Thymocyte Survival by Downregulating p53.

Liang Chen, Daniel P Foreman, Derek B Sant'Angelo, Michael S Krangel

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. YY1Scientific reports · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. YY1 plays an essential role at all stages of B-cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

4 authors at 2 institutions in 1 country.

Liang ChenDepartment of Immunology, Duke University Medical Center, Durham, NC 27710; and.ORCID http://orcid.org/0000-0002-0440-0306
Daniel P ForemanDepartment of Immunology, Duke University Medical Center, Durham, NC 27710; and.ORCID http://orcid.org/0000-0001-6114-9237
Derek B Sant'AngeloChild Health Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ 08901.ORCID http://orcid.org/0000-0002-5510-9367
Michael S KrangelDepartment of Immunology, Duke University Medical Center, Durham, NC 27710; and krang001@mc.duke.edu.ORCID http://orcid.org/0000-0003-1292-254X
Duke Medical Center · USRutgers, The State University of New Jersey · US

Funding

Control Of Tcr Delta And Tcr Alpha RearrangementR37GM041052 · NIGMS · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2006 to 2015
$5.1M
HUMAN GAMMA DELTA T CELL RECEPTORR01GM041052 · NIGMS · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 1989 to 2019
$4.8M
Basic Immunology Training ProgramT32AI052077 · NIAID · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2002 to 2024
$4.2M
The function of PLZF in innate T cellsR01AI083988 · NIAID · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SANT'ANGELO, DEREK B. · 2010 to 2014
$2.2M
NIAID NIH HHS R01 AI083988NIAID NIH HHS T32 AI052077NIGMS NIH HHS R01 GM041052NIGMS NIH HHS R37 GM041052NIGMS NIH HHS R37 GM41052
6 · The paper itself

Abstract

Yin Yang 1 (YY1) is a zinc finger protein that functions as a transcriptional activator or repressor and participates in multiple biological processes, including development and tumorigenesis. To investigate the role of YY1 in developing T cells, we used mouse models that depleted YY1 at two distinct stages of thymocyte development. When YY1 was depleted in CD4(-)CD8(-) double-negative thymocytes, development to the CD4(+)CD8(+) double-positive stage was impaired, due to increased apoptosis that prevented expansion of post-β-selection thymocytes. When YY1 was depleted in double-positive thymocytes, they underwent increased cell-autonomous apoptosis in vitro and displayed a shorter lifespan in vivo, as judged by their ability to undergo secondary Vα-to-Jα recombination. Mechanistically, we found that the increased apoptosis in YY1-deficient thymocytes was attributed to overexpression of p53, because concurrent loss of p53 completely rescued the developmental defects of YY1-deficient thymocytes. These results indicated that YY1 functions as a critical regulator of thymocyte survival and that it does so by suppressing the expression of p53.

Indexed as

AnimalsBlotting, WesternCell SeparationCell SurvivalDisease Models, AnimalFlow CytometryGene Expression RegulationLymphopoiesisMiceMice, KnockoutMice, TransgenicReal-Time Polymerase Chain ReactionThymocytesTranscription, GeneticTumor Suppressor Protein p53YY1 Transcription FactorTumor Suppressor Protein p53Yy1 protein, mouseYY1 Transcription Factor

Identifiers

PMID26843327
PMCPMC4779672
OpenAlexW2261433168

What OpenQuestion holds

Textmetadata
LicenceTDM
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.