Evidence map›Paper›PMID 21695243›Full record

ArticlePLoS pathogens2011

Pathogen recognition receptor signaling accelerates phosphorylation-dependent degradation of IFNAR1.

Juan Qian, Hui Zheng, Wei-Chun Huangfu, Jianghuai Liu, Christopher J Carbone, N Adrian Leu, Darren P Baker, Serge Y Fuchs

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Infection and immunity · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Type III IFNs: Beyond antiviral protection.Seminars in immunology · 2019
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Juan QianDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Hui Zheng
Wei-Chun Huangfu
Jianghuai Liu
Christopher J Carbone
N Adrian Leu
Darren P Baker
Serge Y Fuchs
University of Pennsylvania · USBiogen (United States) · US

Funding

Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
Interferon Responses in Myeloid LeukemiaR01CA142425 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2010 to 2014
$1.6M
NCI NIH HHS CA142425NCI NIH HHS CA92900NCI NIH HHS R01 CA092900NCI NIH HHS R01 CA142425
6 · The paper itself

Abstract

An ability to sense pathogens by a number of specialized cell types including the dendritic cells plays a central role in host's defenses. Activation of these cells through the stimulation of the pathogen-recognition receptors induces the production of a number of cytokines including Type I interferons (IFNs) that mediate the diverse mechanisms of innate immunity. Type I IFNs interact with the Type I IFN receptor, composed of IFNAR1 and IFNAR2 chains, to mount the host defense responses. However, at the same time, Type I IFNs elicit potent anti-proliferative and pro-apoptotic effects that could be detrimental for IFN-producing cells. Here, we report that the activation of p38 kinase in response to pathogen-recognition receptors stimulation results in a series of phosphorylation events within the IFNAR1 chain of the Type I IFN receptor. This phosphorylation promotes IFNAR1 ubiquitination and accelerates the proteolytic turnover of this receptor leading to an attenuation of Type I IFN signaling and the protection of activated dendritic cells from the cytotoxic effects of autocrine or paracrine Type I IFN. In this paper we discuss a potential role of this mechanism in regulating the processes of innate immunity.

Indexed as

Immunity, InnateAnimalsCell LineDendritic CellsHumansInterferon Type IMicep38 Mitogen-Activated Protein KinasesPhosphorylationReceptor, Interferon alpha-betaSignal TransductionUbiquitinationIFNAR1 protein, humanIfnar1 protein, mouseInterferon Type Ip38 Mitogen-Activated Protein KinasesReceptor, Interferon alpha-beta

Identifiers

PMID21695243
PMCPMC3111542
OpenAlexW2099547048

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.