Evidence map›Paper›PMID 9199306›Full record

ArticleMolecular and cellular biology1997

Multiple mechanisms of transcriptional repression by YY1.

K M Galvin, Y Shi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing 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

75 citing papers in PubMed, 185 citations in OpenAlex.

  1. From Thanatos to transcription: the emerging biology of THAP proteins.Cellular and molecular life sciences : CMLS · 2026
    Review
  2. The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Homeostasis Imbalance of YY2 and YY1 Promotes Tumor Growth by Manipulating Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Yin Yang 1 is a potent activator of human T lymphotropic virus type 1 LTR-driven gene expression via RNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

K M GalvinDepartment of Pathology, Harvard Cancer Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
Y Shi
Dana-Farber/Harvard Cancer Center · USHarvard University · US

Funding

TRANSCRIPTIONAL REPRESSION AND ACTIVATION BY YY1R01GM053874 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SHI, YANG · 1996 to 2010
$4.6M
NIGMS NIH HHS GM53874
6 · The paper itself

Abstract

The four C-terminal GLI-Krüppel type zinc fingers of YY1 have been identified as a transcriptional repression domain. Previous reports have proposed DNA-bending and activator-quenching mechanisms for this zinc finger-mediated repression. In addition, previous work indicated that p300 and CBP might be involved in YY1-mediated repression. We have analyzed these possible models for the zinc finger-mediated repression. The role of each zinc finger in the repression and DNA-binding functions was determined by using a structure-and-function approach. We show that zinc finger 2 of YY1 plays a central role in both DNA binding and transcriptional repression. However, a survey of a panel of YY1 mutants indicates that these two functions can be separated, which argues against the DNA-bending model for repression. We show that the physical interaction between YY1 and p300, a coactivator for CREB, is not sufficient for repression of CREB-mediated transcription. Our studies indicate that YY1 functions as an activator-specific repressor. Repression of CTF-1-directed transcription may be accomplished through direct physical interaction between YY1 and this activator. In contrast, physical interaction is not necessary for YY1 to repress Sp1- and CREB-mediated transcription. Rather, the repression likely reflects an ability of YY1 to interfere with communication between these activators and their targets within the general transcription machinery. Taken together, our results suggest that YY1 employs multiple mechanisms to achieve activator-specific repression.

Indexed as

CCAAT-Enhancer-Binding ProteinsTrans-ActivatorsTranscription, GeneticZinc FingersCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsHeLa CellsHumansNFI Transcription FactorsNuclear ProteinsRepressor ProteinsSp1 Transcription FactorStructure-Activity RelationshipTranscription FactorsYY1 Transcription FactorCCAAT-Enhancer-Binding ProteinsCTF-1 transcription factorCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsNFI Transcription FactorsNuclear ProteinsRepressor ProteinsSp1 Transcription FactorTrans-ActivatorsTranscription FactorsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID9199306
PMCPMC232224
OpenAlexW2170249039

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.