Evidence map›Paper›PMID 20215434›Full record

ArticleNucleic acids research2010

Genome-wide analysis of YY2 versus YY1 target genes.

Li Chen, Toshi Shioda, Kathryn R Coser, Mary C Lynch, Chuanwei Yang, Emmett V Schmidt

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Knockdown of YY1 InhibitsInternational journal of molecular sciences · 2022
    Article
  7. Article
  8. Homeostasis Imbalance of YY2 and YY1 Promotes Tumor Growth by Manipulating Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Li ChenCancer Research Center at Massachusetts General Hospital, Boston, MA 02114, USA.
Toshi Shioda
Kathryn R Coser
Mary C Lynch
Chuanwei Yang
Emmett V Schmidt
Cancer Research Center · USHarvard University · USMassachusetts General Hospital · US

Funding

Evolutionary lead optimization for immunotherapy of Marburg & Ebola virusesU01AI070330 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI LACY-HULBERT, ADAM · 2006 to 2010
$4.4M
FUNCTIONS OF CYCLIN D1 IN BREAST CANCERR01CA069069 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHMIDT, EMMETT VANCE · 1997 to 2007
$2.5M
GENES REGULATED BY C-MYCR01CA063117 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHMIDT, EMMETT VANCE · 1994 to 2004
$1.9M
NCI NIH HHS R01-CA63117NCI NIH HHS R01-CA69069NIAID NIH HHS U01 AI070330
6 · The paper itself

Abstract

Yin Yang 1 (YY1) is a critical transcription factor controlling cell proliferation, development and DNA damage responses. Retrotranspositions have independently generated additional YY family members in multiple species. Although Drosophila YY1 [pleiohomeotic (Pho)] and its homolog [pleiohomeotic-like (Phol)] redundantly control homeotic gene expression, the regulatory contributions of YY1-homologs have not yet been examined in other species. Indeed, targets for the mammalian YY1 homolog YY2 are completely unknown. Using gene set enrichment analysis, we found that lentiviral constructs containing short hairpin loop inhibitory RNAs for human YY1 (shYY1) and its homolog YY2 (shYY2) caused significant changes in both shared and distinguishable gene sets in human cells. Ribosomal protein genes were the most significant gene set upregulated by both shYY1 and shYY2, although combined shYY1/2 knock downs were not additive. In contrast, shYY2 reversed the anti-proliferative effects of shYY1, and shYY2 particularly altered UV damage response, platelet-specific and mitochondrial function genes. We found that decreases in YY1 or YY2 caused inverse changes in UV sensitivity, and that their combined loss reversed their respective individual effects. Our studies show that human YY2 is not redundant to YY1, and YY2 is a significant regulator of genes previously identified as uniquely responding to YY1.

Indexed as

Gene Expression RegulationCell LineGene Expression ProfilingGenome, HumanHumansPolymerase Chain ReactionRNA InterferenceTranscription FactorsUltraviolet RaysYY1 Transcription FactorTranscription FactorsYY1 protein, humanYY1 Transcription FactorYY2 protein, human

Identifiers

PMID20215434
PMCPMC2896514
OpenAlexW1991811149

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.