Evidence map›Paper›PMID 35172151›Full record

ArticleCell reports2022

FEZ1 phosphorylation regulates HSPA8 localization and interferon-stimulated gene expression.

Viacheslav Malikov, Nathan Meade, Lacy M Simons, Judd F Hultquist, Mojgan H Naghavi

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 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

5 authors at 1 institution in 1 country.

Viacheslav MalikovDepartment of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Nathan MeadeDepartment of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Lacy M SimonsDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Judd F HultquistDivision of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Mojgan H NaghaviDepartment of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: mojgan.naghavi@northwestern.edu.
Northwestern University · US

Funding

Virology and Immunology Technology CoreP30AI117943 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathryn Rose Macapagal · 2015 to 2026
$38.4M
Functionally Defining HIV-Host Interactions During the Early HIV-1 LifecycleR01AI150998 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BIENIASZ, PAUL D., HOPE, THOMAS · 2020 to 2024
$6.8M
Deciphering the Role of CPSF6 in HIV InfectionR01AI165236 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HULTQUIST, JUDD F · 2021 to 2025
$2.0M
The role of FEZ1 in early HIV-1 infectionR01AI150559 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI NAGHAVI, MOJGAN HOSSEINI · 2019 to 2023
$1.8M
Characterization of the antiviral and nuclear regulatory functions of FEZ1 & NEK1R01GM101975 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI NAGHAVI, MOJGAN HOSSEINI · 2012 to 2016
$1.6M
The Influence of Early Integration Events on HIV Latency and Reactivation PotentialK22AI136691 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HULTQUIST, JUDD F · 2018 to 2019
$269k
NIAID NIH HHS K22 AI136691NIAID NIH HHS P30 AI117943NIAID NIH HHS R01 AI150559NIAID NIH HHS R01 AI150998NIAID NIH HHS R01 AI165236NIGMS NIH HHS R01 GM101975
6 · The paper itself

Abstract

Fasciculation and elongation protein zeta-1 (FEZ1) is a multifunctional kinesin adaptor involved in processes ranging from neurodegeneration to retrovirus and polyomavirus infection. Here, we show that, although modulating FEZ1 expression also impacts infection by large DNA viruses in human microglia, macrophages, and fibroblasts, this broad antiviral phenotype is associated with the pre-induction of interferon-stimulated genes (ISGs) in a STING-independent manner. We further reveal that S58, a key phosphorylation site in FEZ1's kinesin regulatory domain, controls both binding to, and the nuclear-cytoplasmic localization of, heat shock protein 8 (HSPA8), as well as ISG expression. FEZ1- and HSPA8-induced changes in ISG expression further involved changes in DNA-dependent protein kinase (DNA-PK) accumulation in the nucleus. Moreover, phosphorylation of endogenous FEZ1 at S58 was reduced and HSPA8 and DNA-PK translocated to the nucleus in cells stimulated with DNA, suggesting that FEZ1 is a regulatory component of the recently identified HSPA8/DNA-PK innate immune pathway.

Indexed as

Gene Expression RegulationAdaptor Proteins, Signal TransducingAnimalsCell NucleusChlorocebus aethiopsDNA-Activated Protein KinaseDNA VirusesFemaleHEK293 CellsHSC70 Heat-Shock ProteinsHumansImmunity, InnateInterferon Regulatory FactorsInterferonsMembrane ProteinsMicrogliaAdaptor Proteins, Signal TransducingDNA-Activated Protein KinaseFEZ1 protein, humanHSC70 Heat-Shock ProteinsHSPA8 protein, humanInterferon Regulatory FactorsInterferonsMembrane ProteinsNerve Tissue ProteinsPhosphoserinePRKDC protein, humanSTING1 protein, humanSTING ProteinDNA-PKFEZ1HSPA8ISG responses

Identifiers

PMID35172151
PMCPMC8900055
OpenAlexW4213170005

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.