Evidence map›Paper›PMID 19211565›Full record

ArticleThe Journal of biological chemistry2009

Activation of protein kinase C{eta} by type I interferons.

Amanda J Redig, Antonella Sassano, Beata Majchrzak-Kita, Efstratios Katsoulidis, Hui Liu, Jessica K Altman, Eleanor N Fish, Amittha Wickrema, Leonidas C Platanias

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Regulation of interferon-dependent mRNA translation of target genes.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Virus-drug interactions--molecular insight into immunosuppression and HCV.Nature reviews. Gastroenterology & hepatology · 2012
    Review
  13. Article
  14. Article
  15. 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

9 authors at 4 institutions in 2 countries.

Amanda J RedigRobert H. Lurie Comprehensive Cancer Center and Division of Hematology/Oncology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Antonella Sassano
Beata Majchrzak-Kita
Efstratios Katsoulidis
Hui Liu
Jessica K Altman
Eleanor N Fish
Amittha Wickrema
Leonidas C Platanias
Jesse Brown VA Medical Center · USCancer Research Center · USRobert H. Lurie Comprehensive Cancer Center of Northwestern UniversityUniversity Health Network · CA

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
Targeting Novel Protein Complexes for the Treatment of Acute Myeloid LeukemiaR01CA121192 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2006 to 2023
$4.1M
Transcriptional Regulation of Myeloma Cell GrowthR01CA098550 · NCI · UNIVERSITY OF CHICAGO · PI WICKREMA, AMITTHA · 2004 to 2008
$1.2M
Protein Kinase Pathways in Cytokine-SignalingR01CA100579 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2005 to 2008
$1.0M
NCI NIH HHS CA098550NCI NIH HHS CA100579NCI NIH HHS CA121192NCI NIH HHS CA77816
6 · The paper itself

Abstract

Type I interferons (IFNs) are cytokines with diverse biological properties, including antiviral, growth inhibitory, and immunomodulatory effects. Although several signaling pathways are activated during engagement of the type I IFN receptor and participate in the induction of IFN responses, the mechanisms of generation of specific signals for distinct biological effects remain to be elucidated. We provide evidence that a novel member of the protein kinase C (PKC) family of proteins is rapidly phosphorylated and activated during engagement of the type I IFN receptor. In contrast to other members of the PKC family that are also regulated by IFN receptors, PKCeta does not regulate IFN-inducible transcription of interferon-stimulated genes or generation of antiviral responses. However, its function promotes cell cycle arrest and is essential for the generation of the suppressive effects of IFNalpha on normal and leukemic human myeloid (colony-forming unit-granulocyte macrophage) bone marrow progenitors. Altogether, our studies establish PKCeta as a unique element in IFN signaling that plays a key and essential role in the generation of the regulatory effects of type I IFNs on normal and leukemic hematopoiesis.

Indexed as

AnimalsAntigens, CDAntigens, CD34Cell Line, TumorEnzyme ActivationHumansInterferon Type IIsoenzymesLeukemia, MyeloidMyeloid Progenitor CellsProtein Kinase CProtein Kinase C-alphaProtein Kinase C betaProtein Kinase C-lambdaReceptors, TransferrinRNA, Small InterferingAntigens, CDAntigens, CD34CD71 antigenInterferon Type IIsoenzymesProtein Kinase CProtein Kinase C-alphaProtein Kinase C betaprotein kinase C etaProtein Kinase C-lambdaReceptors, TransferrinRNA, Small Interfering

Identifiers

PMID19211565
PMCPMC2667717
OpenAlexW2045706265

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.