Evidence map›Paper›PMID 25049393›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Regulatory effects of SKAR in interferon α signaling and its role in the generation of type I IFN responses.

Barbara Kroczynska, Swarna Mehrotra, Beata Majchrzak-Kita, Ahmet Dirim Arslan, Jessica K Altman, Brady L Stein, Brandon McMahon, Piotr Kozlowski, Philipp J Kahle, Elizabeth A Eklund and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. 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
0.4field-weighted citation impact, top 34% 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, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Deciphering GRINA/Lifeguard1: Nuclear Location, CaInternational journal of molecular sciences · 2019
    Review
  6. Article
  7. Type I Interferon-Mediated Induction of Antiviral Genes and Proteins Fails to Protect Cells from the Cytopathic Effects of Sendai Virus Infection.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Article
  8. Article
  9. Article
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

12 authors at 4 institutions in 4 countries.

Barbara KroczynskaRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;
Swarna MehrotraRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;
Beata Majchrzak-KitaToronto General Research Institute, University Health Network, andDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S 2J7;
Ahmet Dirim ArslanRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;
Jessica K AltmanRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;Division of Hematology/Oncology, Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612;
Brady L SteinRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;
Brandon McMahonRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;
Piotr KozlowskiDepartment of Molecular Biology, Faculty of Biology, University of Warsaw, 02-096, Warsaw, Poland; and.
Philipp J KahleDepartment of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, 72076 Tuebingen, Germany.
Elizabeth A EklundRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;Division of Hematology/Oncology, Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612;
Eleanor N FishToronto General Research Institute, University Health Network, andDepartment of Immunology, University of Toronto, Toronto, ON, Canada M5S 2J7;
Leonidas C PlataniasRobert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;Division of Hematology/Oncology, Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612; l-platanias@northwestern.edu.
Northwestern University · USUniversity Health Network · CAHertie Institute for Clinical Brain Research · DEUniversity of Warsaw · PL

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Signal Transduction of Type I Interferons in Malignant CellsR01CA077816 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 1998 to 2024
$6.6M
TRAINING PROGRAM IN SIGNAL TRANSDUCTION AND CANCERT32CA070085 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1997 to 2026
$5.7M
Interferon-induced SLFNs and tumorigenesisR01CA161796 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
NCI NIH HHS CA15566NCI NIH HHS CA161796NCI NIH HHS CA77816NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA161796NCI NIH HHS T32 CA070085
6 · The paper itself

Abstract

We provide evidence that S6 kinase 1 (S6K1) Aly/REF-like target (SKAR) is engaged in IFN-α signaling and plays a key role in the generation of IFN responses. Our data demonstrate that IFN-α induces phosphorylation of SKAR, which is mediated by either the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-specific manner. This type I IFN-inducible phosphorylation of SKAR results in enhanced interaction with the eukaryotic initiation factor (eIF)4G and recruitment of activated RSK1 to 5' cap mRNA. Our studies also establish that SKAR is present in cap-binding CBP80 immune complexes and that this interaction is mediated by eIF4G. We demonstrate that inducible protein expression of key IFN-α-regulated protein products such as ISG15 and p21(WAF1/CIP1) requires SKAR activity. Importantly, our studies define a requirement for SKAR in the generation of IFN-α-dependent inhibitory effects on malignant hematopoietic progenitors from patients with chronic myeloid leukemia or myeloproliferative neoplasms. Taken altogether, these findings establish critical and essential roles for SKAR in the regulation of mRNA translation of IFN-sensitive genes and induction of IFN-α biological responses.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21CytokinesGuanosineHumansInterferon-alphaMiceNuclear Cap-Binding Protein ComplexNuclear ProteinsPhosphorylationRibosomal Protein S6 Kinases, 90-kDaRNA-Binding ProteinsUbiquitins7-methylguanosineAntineoplastic AgentsCyclin-Dependent Kinase Inhibitor p21CytokinesGuanosineInterferon-alphaISG15 protein, humanNuclear Cap-Binding Protein ComplexNuclear ProteinsPOLDIP3 protein, humanRibosomal Protein S6 Kinases, 90-kDaRNA-Binding ProteinsUbiquitins

Identifiers

PMID25049393
PMCPMC4128135
OpenAlexW2077260651

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.