Evidence map›Paper›PMID 28615693›Full record

ArticleScientific reports2017

The CCR4-NOT complex contributes to repression of Major Histocompatibility Complex class II transcription.

Alfonso Rodríguez-Gil, Olesja Ritter, Vera V Saul, Jochen Wilhelm, Chen-Yuan Yang, Rudolf Grosschedl, Yumiko Imai, Keiji Kuba, Michael Kracht, M Lienhard Schmitz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 34 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

10 authors at 5 institutions in 2 countries.

Alfonso Rodríguez-GilInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany. Alfonso.Rodriguez-Gil@biochemie.med.uni-giessen.de.ORCID 0000-0003-4430-077X
Olesja RitterInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany.
Vera V SaulInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany.
Jochen WilhelmDepartment of Pathology, Universities of Giessen and Marburg Lung Center, Excellence Cluster Cardio-Pulmonary System, D-35392, Giessen, Germany.
Chen-Yuan YangMax-Planck Institute for Immunobiology and Epigenetics, D-79108, Freiburg, Germany.
Rudolf GrosschedlMax-Planck Institute for Immunobiology and Epigenetics, D-79108, Freiburg, Germany.
Yumiko ImaiDepartment of Biochemistry and Metabolic Sciences, Akita University Graduate School of Medicine, Akita, 010-8543, Japan.
Keiji KubaDepartment of Biochemistry and Metabolic Sciences, Akita University Graduate School of Medicine, Akita, 010-8543, Japan.
Michael KrachtRudolf-Buchheim-Institute of Pharmacology, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany.
M Lienhard SchmitzInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392, Giessen, Germany. Lienhard.Schmitz@biochemie.med.uni-giessen.de.
German Center for Lung Research · DEAkita University · JPJustus-Liebig-Universität Gießen · DEMax Planck Institute of Immunobiology and Epigenetics · DEUniversities of Giessen and Marburg Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The multi-subunit CCR4 (carbon catabolite repressor 4)-NOT (Negative on TATA) complex serves as a central coordinator of all different steps of eukaryotic gene expression. Here we performed a systematic and comparative analysis of cells where the CCR4-NOT subunits CNOT1, CNOT2 or CNOT3 were individually downregulated using doxycycline-inducible shRNAs. Microarray experiments showed that downregulation of either CNOT subunit resulted in elevated expression of major histocompatibility complex class II (MHC II) genes which are found in a gene cluster on chromosome 6. Increased expression of MHC II genes after knock-down or knock-out of either CNOT subunit was seen in a variety of cell systems and also in naïve macrophages from CNOT3 conditional knock-out mice. CNOT2-mediated repression of MHC II genes occurred also in the absence of the master regulator class II transactivator (CIITA) and did not cause detectable changes of the chromatin structure at the chromosomal MHC II locus. CNOT2 downregulation resulted in an increased de novo transcription of mRNAs whereas tethering of CNOT2 to a regulatory region governing MHC II expression resulted in diminished transcription. These results expand the known repertoire of CCR4-NOT members for immune regulation and identify CNOT proteins as a novel group of corepressors restricting class II expression.

Indexed as

Down-RegulationTranscription, GeneticAnimalsCell LineGene Regulatory NetworksHistocompatibility Antigens Class IIHumansMiceRepressor ProteinsTranscription FactorsCNOT1 protein, humanCNOT2 protein, humanCNOT3 protein, humanHistocompatibility Antigens Class IIRepressor ProteinsTranscription Factors

Identifiers

PMID28615693
PMCPMC5471237
OpenAlexW2622970893

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.