Evidence map›Paper›PMID 15269344›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

CCAAT displacement protein/cut homolog recruits G9a histone lysine methyltransferase to repress transcription.

Hitomi Nishio, Martin J Walsh

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

90 citing papers in PubMed, 146 citations in OpenAlex.

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30 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.

Hitomi NishioDepartment of Pediatrics, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Martin J Walsh
Icahn School of Medicine at Mount Sinai · USRockefeller University · US

Funding

Regulation of CFTR gene expressionR01HL067099 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI WALSH, MARTIN JOHN · 2001 to 2004
$1.2M
NHLBI NIH HHS HL67099NHLBI NIH HHS R01 HL067099
6 · The paper itself

Abstract

CCAAT displacement protein/cut homolog (CDP/cut) is a highly conserved homeodomain protein that contains three cut repeat sequences. CDP/cut is a transcriptional factor for many diverse cellular and viral genes that are involved in most cellular processes, including differentiation, development, and proliferation. Here, we report that CDP/cut interacts with a histone lysine methyltransferase (HKMT), G9a, in vivo and in vitro. The deletion of the cut repeats within CDP/cut abrogates the interaction with G9a. The transcriptional repressor function of CDP/cut is mediated through HKMT activity of G9a associated with CDP/cut. We show that the recruitment of G9a to the human p21(waf1/cdi1) promoter is contingent on the interaction with CDP/cut, and CDP/cut is directly associated with an increase in the methylation in vivo of Lys-9 in histone H3 within the CDP/cut-regulatory region of the p21(waf1/cdi1) promoter. The endogenous level of p21(waf1/cdi1) expression is repressed through CDP/cut and mediated by HKMT activity of G9a. Furthermore, we report the identification of G9a as a component of CDP/cut complex. G9a colocalizes with CDP/cut in the nucleus. These results indicate that G9a functions as a transcriptional corepressor in association with a CDP/cut complex. These studies now reveal the interaction of G9a with a sequence-specific transcription factor that regulates gene repression through CDP/cut.

Indexed as

Cell NucleusCells, CulturedChromatinCyclin-Dependent Kinase Inhibitor p21CyclinsHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHomeodomain ProteinsHumansIn Vitro TechniquesLysineNuclear ProteinsPromoter Regions, GeneticProtein MethyltransferasesRepressor ProteinsTranscription FactorsCDKN1A protein, humanChromatinCUX1 protein, humanCyclin-Dependent Kinase Inhibitor p21CyclinsHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHomeodomain ProteinsLysineNuclear ProteinsProtein MethyltransferasesRepressor ProteinsTranscription Factors

Identifiers

PMID15269344
PMCPMC509191
OpenAlexW2158202559

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.