Evidence map›Paper›PMID 21343339›Full record

ArticleMolecular and cellular biology2011

Functional analysis of KAP1 genomic recruitment.

Sushma Iyengar, Alexey V Ivanov, Victor X Jin, Frank J Rauscher, Peggy J Farnham

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Article
  3. DurableMolecular therapy. Nucleic acids · 2025
    Article
  4. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Nuclear mProtein & cell · 2021
    Article
  17. Review
  18. Article
  19. Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma.International journal of molecular sciences · 2020
    Review
  20. Article

24 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

5 authors at 5 institutions in 1 country.

Sushma IyengarDepartment of Biochemistry & Molecular Biology, Norris Comprehensive Cancer Center, 1450 Biggy Street, NRT 6503, Mail Code 9601, University of Southern California, Los Angeles, CA 90089, USA.
Alexey V Ivanov
Victor X Jin
Frank J Rauscher
Peggy J Farnham
The Ohio State University · USThe Wistar Institute · USUniversity of California, Davis · USUniversity of Southern California · USWest Virginia University · US

Funding

THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
Production Center for Global Mapping of Regulatory ElementsU54HG004558 · NHGRI · YALE UNIVERSITY · PI SNYDER, MICHAEL P. · 2007 to 2011
$15.4M
TRANSCRIPTIONAL REGULATION OF GROWTH-RELATED GENESR01CA045240 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI FARNHAM, PEGGY J · 1992 to 2011
$3.4M
TRANSCRIPTIONAL REGULATION OF GROWTH-RELATED GENESR29CA045240 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI FARNHAM, PEGGY J · 1987 to 1991
–
NCI NIH HHS CA45240NCI NIH HHS R01 CA045240NHGRI NIH HHS U54 HG004558NHGRI NIH HHS U54HG004558
6 · The paper itself

Abstract

TRIM28 (KAP1) is upregulated in many cancers and has been implicated in both transcriptional activation and repression. Using chromatin immunoprecipitation and sequencing, we show that KAP1 binding sites fall into several categories, specifically, the 3' coding exons of zinc finger (ZNF) genes and promoter regions of ZNFs and other genes. The currently accepted model is that KAP1 is recruited to the genome via interaction of its N-terminal RBCC domain with KRAB ZNFs (KRAB domain containing ZNFs). To determine whether the interaction of KAP1 with KRAB ZNFs is the mechanism by which KAP1 is recruited to genomic binding sites, we analyzed stable cell lines that express tagged wild-type and mutant KAP1. Surprisingly, deletion of the RBCC domain abolished KAP1 binding to the 3' exons of ZNF genes but KAP1 binding to promoter regions was unaffected. Using KAP1 knockdown cells, we showed that the genes most responsive to KAP1 were not ZNF genes but instead were either indirect targets or had KAP1 bound 10 to 100 kb from the transcription start site. Therefore, our studies suggest that KAP1 plays a role distinct from transcriptional regulation at the majority of its strongest binding sites.

Indexed as

Binding SitesCell LineCell Line, TumorChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneGene Expression RegulationHistone-Lysine N-MethyltransferaseHistonesHumansMutationPromoter Regions, GeneticProtein MethyltransferasesRepressor ProteinsTripartite Motif-Containing Protein 28Zinc FingersChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistone-Lysine N-MethyltransferaseHistonesProtein MethyltransferasesRepressor ProteinsSETDB1 protein, humanTRIM28 protein, humanTripartite Motif-Containing Protein 28ZNF350 protein, human

Identifiers

PMID21343339
PMCPMC3133220
OpenAlexW2137027550

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.