Evidence map›Paper›PMID 16322561›Full record

ArticleGenes & development2005

NIR is a novel INHAT repressor that modulates the transcriptional activity of p53.

Philip Hublitz, Natalia Kunowska, Ulrich P Mayer, Judith M Müller, Kristina Heyne, Na Yin, Claudia Fritzsche, Cecilia Poli, Laurent Miguet, Ingo W Schupp and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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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

16 authors at 6 institutions in 2 countries.

Philip HublitzFrauenklinik der Albert-Ludwigs-Universität Freiburg, Zentrale Klinische Forschung, D-79106 Freiburg, Germany.
Natalia Kunowska
Ulrich P Mayer
Judith M Müller
Kristina Heyne
Na Yin
Claudia Fritzsche
Cecilia Poli
Laurent Miguet
Ingo W Schupp
Leo A van Grunsven
Noëlle Potiers
Alain van Dorsselaer
Eric Metzger
Klaus Roemer
Roland Schüle
University of Freiburg · DEKU Leuven · BEGerman Cancer Research Center · DEDKFZ-ZMBH Alliance · DEHeidelberg University · DEVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most transcriptional repression pathways depend on the targeted deacetylation of histone tails. In this report, we characterize NIR, a novel transcriptional corepressor with inhibitor of histone acetyltransferase (INHAT) activity. NIR (Novel INHAT Repressor) is ubiquitously expressed throughout embryonic development and adulthood. NIR is a potent transcriptional corepressor that is not blocked by histone deacetylase inhibitors and is capable of silencing both basal and activator-driven transcription. NIR directly binds to nucleosomes and core histones and prevents acetylation by histone acetyltransferases, thus acting as a bona fide INHAT. Using a tandem affinity purification approach, we identified the tumor suppressor p53 as a NIR-interacting partner. Association of p53 and NIR was verified in vitro and in vivo. Upon recruitment by p53, NIR represses transcription of both p53-dependent reporters and endogenous target genes. Knock-down of NIR by RNA interference significantly enhances histone acetylation at p53-regulated promoters. Moreover, p53-dependent apoptosis is robustly increased upon depletion of NIR. In summary, our findings describe NIR as a novel INHAT that plays an important role in the control of p53 function.

Indexed as

Transcription, GeneticAnimalsApoptosisGene Expression RegulationHistone AcetyltransferasesHumansMiceMice, KnockoutPromoter Regions, GeneticProtein Interaction MappingRepressor ProteinsRNA InterferenceTumor Suppressor Protein p53Histone AcetyltransferasesNIR protein, mouseNOC2L protein, humanRepressor ProteinsTumor Suppressor Protein p53

Identifiers

PMID16322561
PMCPMC1315397
OpenAlexW2145394000

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.