Evidence map›Paper›PMID 27122605›Full record

ArticleMolecular biology of the cell2016

HIPK family kinases bind and regulate the function of the CCR4-NOT complex.

Alfonso Rodriguez-Gil, Olesja Ritter, Juliane Hornung, Hilda Stekman, Marcus Krüger, Thomas Braun, Elisabeth Kremmer, Michael Kracht, M Lienhard Schmitz

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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  9. Reparameterization of PAM50 Expression Identifies Novel Breast Tumor Dimensions and Leads to Discovery of a Genome-Wide Significant Breast Cancer Locus atCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
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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

9 authors at 3 institutions in 1 country.

Alfonso Rodriguez-GilInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392 Giessen, Germany.
Olesja RitterInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392 Giessen, Germany.
Juliane HornungInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392 Giessen, Germany.
Hilda StekmanInstitute of Biochemistry, Medical Faculty, Justus-Liebig-University, Member of the German Center for Lung Research, D-35392 Giessen, Germany.
Marcus KrügerMax Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany.
Thomas BraunMax Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany.
Elisabeth KremmerInstitute of Molecular Immunology, Helmholtz Center Munich, German Research Center for Environmental Health, D-81377 Munich; Germany.
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 · DEMax Planck Institute for Heart and Lung Research · DEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine/threonine kinase HIPK2 functions as a regulator of developmental processes and as a signal integrator of a wide variety of stress signals, such as DNA damage, hypoxia, and reactive oxygen intermediates. Because the kinase is generated in a constitutively active form, its expression levels are restricted by a variety of different mechanisms. Here we identify the CCR4-NOT complex as a new regulator of HIPK2 abundance. Down-regulation or knockout of the CCR4-NOT complex member CNOT2 leads to reduced HIPK2 protein levels without affecting the expression level of HIPK1 or HIPK3. A fraction of all HIPK family members associates with the CCR4-NOT components CNOT2 and CNOT3. HIPKs also phosphorylate the CCR4-NOT complex, a feature that is shared with their yeast progenitor kinase, YAK1. Functional assays reveal that HIPK2 and HIPK1 restrict CNOT2-dependent mRNA decay. HIPKs are well known regulators of transcription, but the mutual regulation between CCR4-NOT and HIPKs extends the regulatory potential of these kinases by enabling posttranscriptional gene regulation.

Indexed as

Carrier ProteinsDNA DamageHumansNuclear Receptor Subfamily 4, Group A, Member 2PhosphorylationProtein Serine-Threonine KinasesReceptors, CCR4Repressor ProteinsSignal TransductionTranscription FactorsTwo-Hybrid System TechniquesCarrier ProteinsCCR4 protein, humanCNOT2 protein, humanCNOT3 protein, humanHIPK2 protein, humanNR4A2 protein, humanNuclear Receptor Subfamily 4, Group A, Member 2Protein Serine-Threonine KinasesReceptors, CCR4Repressor ProteinsTranscription Factors

Identifiers

PMID27122605
PMCPMC4907730
OpenAlexW2342798578

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.