Evidence map›Paper›PMID 22550181›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Regulatory effects of mTORC2 complexes in type I IFN signaling and in the generation of IFN responses.

Surinder Kaur, Antonella Sassano, Beata Majchrzak-Kita, Darren P Baker, Bing Su, Eleanor N Fish, Leonidas C Platanias

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. 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
3.2field-weighted citation impact, top 7% 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, 49 citations in OpenAlex.

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  15. 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
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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 5 institutions in 2 countries.

Surinder KaurRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Northwestern University Medical School, Chicago, IL 60611, USA.
Antonella Sassano
Beata Majchrzak-Kita
Darren P Baker
Bing Su
Eleanor N Fish
Leonidas C Platanias
Jesse Brown VA Medical Center · USUniversity of Toronto · CABiogen (United States) · USNorthwestern University · USYale University · US

Funding

Signal Transduction of Type I Interferons in Malignant CellsR01CA077816 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 1998 to 2024
$6.6M
Interferon-induced SLFNs and tumorigenesisR01CA161796 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
CIHR MOP 1504NCI NIH HHS CA15566NCI NIH HHS CA161796NCI NIH HHS CA77816NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA161796
6 · The paper itself

Abstract

IFNs transduce signals by binding to cell surface receptors and activating cellular pathways and regulatory networks that control transcription of IFN-stimulated genes (ISGs) and mRNA translation, leading to generation of protein products that mediate biological responses. Previous studies have shown that type I IFN receptor-engaged pathways downstream of AKT and mammalian target of rapamycin complex (mTORC) 1 play important roles in mRNA translation of ISGs and the generation of IFN responses, but the roles of mTORC2 complexes in IFN signaling are unknown. We provide evidence that mTORC2 complexes control IFN-induced phosphorylation of AKT on serine 473 and their function is ultimately required for IFN-dependent gene transcription via interferon-stimulated response elements. We also demonstrate that such complexes exhibit regulatory effects on other IFN-dependent mammalian target of rapamycin-mediated signaling events, likely via engagement of the AKT/mTORC1 axis, including IFN-induced phosphorylation of S6 kinase and its effector rpS6, as well as phosphorylation of the translational repressor 4E-binding protein 1. We also show that induction of ISG protein expression and the generation of antiviral responses are defective in Rictor and mLST8-KO cells. Together, our data provide evidence for unique functions of mTORC2 complexes in the induction of type I IFN responses and suggest a critical role for mTORC2-mediated signals in IFN signaling.

Indexed as

AnimalsCarrier ProteinsGene Expression RegulationHeLa CellsHumansImmunoblottingInterferonsLuciferasesMechanistic Target of Rapamycin Complex 2MiceMultiprotein ComplexesPhosphorylationProto-Oncogene Proteins c-aktRapamycin-Insensitive Companion of mTOR ProteinReverse Transcriptase Polymerase Chain ReactionRibosomal Protein S6Carrier ProteinsInterferonsLuciferasesMechanistic Target of Rapamycin Complex 2Multiprotein ComplexesProto-Oncogene Proteins c-aktRapamycin-Insensitive Companion of mTOR ProteinRibosomal Protein S6Ribosomal Protein S6 Kinasesribosomal protein S6, mouserictor protein, mouseTOR Serine-Threonine KinasesTrans-Activators

Identifiers

PMID22550181
PMCPMC3356630
OpenAlexW2124597799

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.