Evidence map›Paper›PMID 24469448›Full record

ArticleThe Journal of biological chemistry2014

Critical roles for Rictor/Sin1 complexes in interferon-dependent gene transcription and generation of antiproliferative responses.

Surinder Kaur, Barbara Kroczynska, Bhumika Sharma, Antonella Sassano, Ahmet Dirim Arslan, Beata Majchrzak-Kita, Brady L Stein, Brandon McMahon, Jessica K Altman, Bing Su and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  4. Trisomy 21 dysregulates T cell lineages toward an autoimmunity-prone state associated with interferon hyperactivity.Proceedings of the National Academy of Sciences of the United States of America · 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

13 authors at 4 institutions in 3 countries.

Surinder KaurRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Barbara KroczynskaRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Bhumika SharmaRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Antonella SassanoRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Ahmet Dirim ArslanRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Beata Majchrzak-KitaToronto Research Institute, University Health Network and Department of Immunology, University of Toronto, Toronto, Ontario M5S 2J7, Canada.
Brady L SteinRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Brandon McMahonRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Jessica K AltmanRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611; Division of Hematology-Oncology, Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois 60612.
Bing SuDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520.
Raffaele A CalogeroDepartment of Biotechnology and Health Sciences, University of Turin, 8 Turin, Italy.
Eleanor N FishToronto Research Institute, University Health Network and Department of Immunology, University of Toronto, Toronto, Ontario M5S 2J7, Canada.
Leonidas C PlataniasRobert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611; Division of Hematology-Oncology, Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois 60612. Electronic address: l-platanias@northwestern.edu.
Northwestern University · USUniversity Health Network · CAUniversity of Turin · ITYale University · US

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
Mnk Pathways and IFN-responses in Malignant CellsR01CA155566 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
Interferon-induced SLFNs and tumorigenesisR01CA161796 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2011 to 2015
$1.6M
NCI NIH HHS CA155566NCI NIH HHS CA161796NCI NIH HHS CA77816NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA155566NCI NIH HHS R01 CA161796NCI NIH HHS T32 CA070085
6 · The paper itself

Abstract

We provide evidence that type I IFN-induced STAT activation is diminished in cells with targeted disruption of the Rictor gene, whose protein product is a key element of mTOR complex 2. Our studies show that transient or stable knockdown of Rictor or Sin1 results in defects in activation of elements of the STAT pathway and reduced STAT-DNA binding complexes. This leads to decreased expression of several IFN-inducible genes that mediate important biological functions. Our studies also demonstrate that Rictor and Sin1 play essential roles in the generation of the suppressive effects of IFNα on malignant erythroid precursors from patients with myeloproliferative neoplasms. Altogether, these findings provide evidence for critical functions for Rictor/Sin1 complexes in type I IFN signaling and the generation of type I IFN antineoplastic responses.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntineoplastic AgentsCarrier ProteinsCells, CulturedFibroblastsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHematopoietic Stem CellsHumansInterferon Type IMicePhosphorylationPolycythemia VeraRapamycin-Insensitive Companion of mTOR ProteinSignal TransductionAdaptor Proteins, Signal TransducingAntineoplastic AgentsCarrier ProteinsInterferon Type IMapkap1 protein, mouseRapamycin-Insensitive Companion of mTOR Proteinrictor protein, mouseAkt PKBAntiviral AgentsCell SignalingCytokines/InterferonGene RegulationInterferonSignal Transduction

Identifiers

PMID24469448
PMCPMC3945321
OpenAlexW2054702239

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.