Evidence map›Paper›PMID 32849638›Full record

ArticleFrontiers in immunology2020

HDAC6 Mediates Poly (I:C)-Induced TBK1 and Akt Phosphorylation in Macrophages.

Yan Wang, Ke Wang, Jian Fu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  5. Article
  6. Lack of effect from genetic deletion of Hdac6 in a humanized mouse model of CMT2D.Journal of the peripheral nervous system : JPNS · 2024
    Article
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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

3 authors at 2 institutions in 2 countries.

Yan WangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
Ke WangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
Jian FuDepartment of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, KY, United States.
University of Kentucky · USSecond Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are derived from monocytes in the bone marrow and play an important role in anti-viral innate immune responses. Macrophages produce cytokines such as interferons and IL-10 upon viral infection to modulate anti-viral immune responses. Type I interferons (IFNs) promote anti-viral defense. IL-10 is a suppressor cytokine that down-regulates anti-viral immune responses. HDAC6 is a tubulin deacetylase that can modulate microtubule dynamics and microtubule-mediated cell signaling pathways. In the present study, we investigated the potential role of HDAC6 in macrophage anti-viral responses by examining poly (I:C)-induced IFN-β and IL-10 production in mouse bone marrow-derived macrophages (BMDMs). We also investigated the role of HDAC6 in poly (I:C)-induced anti-viral signaling such as TBK1, GSK-3β, and Akt activation in mouse BMDMs. Our data showed that HDAC6 deletion enhanced poly (I:C)-induced INF-β expression in macrophages by up-regulating TBK1 activity and eliminating the inhibitory regulation of GSK-3β. Furthermore, HDAC6 deletion inhibited poly (I:C)-induced suppressor cytokine IL-10 production in the BMDMs, which was associated with the inhibition of Akt activation. Our results suggest that HDAC6 modulates IFN-β and IL-10 production in macrophages through its regulation of TBK1, GSK-3β, and Akt signaling. HDAC6 could act as a suppressor of anti-viral innate immune responses in macrophages.

Indexed as

AnimalsGene Expression RegulationHistone Deacetylase 6Immunity, InnateMacrophagesMiceMice, Inbred C57BLMice, KnockoutPhosphorylationPoly I-CProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktVirus DiseasesHdac6 protein, mouseHistone Deacetylase 6Poly I-CProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTbk1 protein, mouseacetylationcytokineinfectioninnate immunitymicrotubule

Identifiers

PMID32849638
PMCPMC7431618
OpenAlexW3048794763

What OpenQuestion holds

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LicenceCC BY
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.