Evidence map›Paper›PMID 27909056›Full record

ArticleThe Journal of biological chemistry2017

Interferons Induce Expression of SAMHD1 in Monocytes through Down-regulation of miR-181a and miR-30a.

Maximilian Riess, Nina V Fuchs, Adam Idica, Matthias Hamdorf, Egbert Flory, Irene Munk Pedersen, Renate König

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 54 citations in OpenAlex.

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  18. Isolation, Transfection, and Culture of Primary Human Monocytes.Journal of visualized experiments : JoVE · 2019
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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

7 authors at 3 institutions in 2 countries.

Maximilian RiessFrom the Host-Pathogen Interactions Group and.
Nina V FuchsFrom the Host-Pathogen Interactions Group and.
Adam Idicathe Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697.
Matthias Hamdorfthe Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697.
Egbert Florythe Division of Medical Biotechnology, Paul-Ehrlich-Institute, 63225 Langen, Germany.
Irene Munk Pedersenthe Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697.
Renate KönigFrom the Host-Pathogen Interactions Group and renate.koenig@pei.de.
University of California, Irvine · USPaul Ehrlich Institut · DESanford Burnham Prebys Medical Discovery Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SAMHD1 is a phosphohydrolase maintaining cellular dNTP homeostasis but also acts as a critical regulator in innate immune responses due to its antiviral activity and association with autoimmune disease, leading to aberrant activation of interferon. SAMHD1 expression is differentially regulated by interferon in certain primary cells, but the underlying mechanism is not understood. Here, we report a detailed characterization of the promotor region, the 5'- and 3'-untranslated region (UTR) of SAMHD1, and the mechanism responsible for the cell type-dependent up-regulation of SAMHD1 protein by interferon. We demonstrate that induction of SAMHD1 by type I and II interferons depends on 3'-UTR post-transcriptional regulation, whereas the promoter drives basal expression levels. We reveal novel functional target sites for the microRNAs miR-181a, miR-30a, and miR-155 in the SAMHD1 3'-UTR. Furthermore, we demonstrate that down-regulation of endogenous miR-181a and miR-30a levels inversely correlates with SAMHD1 protein up-regulation upon type I and II interferon stimulation in primary human monocytes. These miRNAs are not modulated by interferon in macrophages or dendritic cells, and consequently protein levels of SAMHD1 remain unchanged. These results suggest that SAMHD1 is a non-classical interferon-stimulated gene regulated through cell type-dependent down-regulation of miR-181a and miR-30a in innate sentinel cells.

Indexed as

3' Untranslated RegionsBase SequenceCells, CulturedDendritic CellsDown-RegulationHumansInterferon-gammaInterferon Type IMicroRNAsMonocytesMonomeric GTP-Binding ProteinsSAM Domain and HD Domain-Containing Protein 13' Untranslated RegionsInterferon-gammaInterferon Type IMicroRNAsMIrn181 microRNA, humanMIRN30b microRNA, humanMonomeric GTP-Binding ProteinsSAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, humandNTPasehuman immunodeficiency virus (HIV)innate immunityinnate sentinel cellsinterferoninterferon stimulated genemicroRNA (miRNA)promoterregulation of expressionSAM domain and HD domain-containing protein 1 (SAMHD1)

Identifiers

PMID27909056
PMCPMC5217685
OpenAlexW2558825847

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.