Evidence map›Paper›PMID 19074285›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

GRIP1-associated SET-domain methyltransferase in glucocorticoid receptor target gene expression.

Yurii Chinenov, Maria A Sacta, Anna R Cruz, Inez Rogatsky

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. The SUV4-20H Histone Methyltransferases in Health and Disease.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Role of transcriptional coregulator GRIP1 in the anti-inflammatory actions of glucocorticoids.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

4 authors at 3 institutions in 1 country.

Yurii ChinenovHospital for Special Surgery, Department of Microbiology and Immunology, Weill Medical College of Cornell University, 535 E70th Street, Research Building Rm. 425, New York, NY 10021, USA.
Maria A Sacta
Anna R Cruz
Inez Rogatsky
Cornell University · USHospital for Special Surgery · USUniversity of California, San Francisco · US

Funding

GENE REGULATION BY STEROID RECEPTOR PROTEINSR01CA020535 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YAMAMOTO, KEITH ROBERT · 1985 to 2018
$8.9M
Mechanisms of Immunosuppressive Actions of GlucocorticoidsR01AI068820 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI ROGATSKY, INEZ · 2007 to 2011
$2.3M
RHEUMATOLOGY TRAININGT32AR007517 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 1986 to 2014
$2.2M
GENE REGULATION BY STEROID RECEPTOR PROTEINSR37CA020535 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI YAMAMOTO, KEITH ROBERT · 1990 to 1998
–
NCI NIH HHS CA20535NCI NIH HHS R01 CA020535NCI NIH HHS R37 CA020535NIAID NIH HHS AI068820NIAID NIH HHS R01 AI068820NIAMS NIH HHS T32 AR007517NIAMS NIH HHS T32 AR07517
6 · The paper itself

Abstract

Transcriptional regulators such as the glucocorticoid receptor (GR) recruit multiple cofactors to activate or repress transcription. Although most cofactors are intrinsically bifunctional, little is known about the molecular mechanisms dictating the specific polarity of regulation. Furthermore, chromatin modifications thought to be confined to silent loci appear in actively transcribed genes suggesting that similar enzymatic activities may mediate constitutive and transient chromatin states. GRIP1, a GR ligand-dependent coregulator of the p160 family can potentiate or inhibit transcription but the molecular contexts and mechanisms that enable GRIP1 corepressor activity are poorly understood. In a yeast 2-hybrid screen with GRIP1 repression domain (RD)-containing fragment, we repeatedly isolated the C-terminal region of a SET domain-containing protein subsequently identified as histone H4 lysine 20 trimethyltransferase, Suv4-20h1. We cloned a full-length Suv4-20h1 and dissected its interaction with GRIP1 in yeast, in vitro, and in mammalian cells. Strict nuclear localization and high salt concentration required for Suv4-20h1 extraction were consistent with its tight association with chromatin. Overexpression of Suv4-20h1 in human U2OS and A549 cells expressing integrated and endogenous GR, respectively, antagonized ligand-dependent induction of a subset of GR target genes, whereas Suv4-20h1 siRNA-mediated depletion had a reciprocal effect. Inhibition of GR transactivation required both the GRIP1 interacting region of Suv4-20h1 and its catalytic activity. Thus, Suv4-20h1 known exclusively as a factor involved in constitutive heterochromatin maintenance, actively participates in hormone-dependent transcriptional regulation affecting GR target gene expression in a promoter- and cell type-specific manner.

Indexed as

Gene Expression RegulationBinding SitesCarrier ProteinsCell LineCloning, MolecularHistone-Lysine N-MethyltransferaseHumansNerve Tissue ProteinsProtein BindingProtein Structure, TertiaryReceptors, GlucocorticoidTranscription, GeneticCarrier ProteinsGRIP1 protein, humanHistone-Lysine N-MethyltransferaseNerve Tissue ProteinsReceptors, Glucocorticoid

Identifiers

PMID19074285
PMCPMC2629346
OpenAlexW2054290031

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.