Evidence map›Paper›PMID 26046815›Full record

ArticleCancer biology & therapy2015

Type 1 interferons contribute to the clearance of senescent cell.

Yuliya V Katlinskaya, Christopher J Carbone, Qiujing Yu, Serge Y Fuchs

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-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

13 citing papers in PubMed, 19 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Yuliya V Katlinskayaa Department of Biomedical Sciences ; School of Veterinary Medicine ; University of Pennsylvania ; Philadelphia , PA USA.
Christopher J Carbone
Qiujing Yu
Serge Y Fuchs
California University of Pennsylvania · USPhiladelphia University · US

Funding

UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KOUMENIS, CONSTANTINOS · 2013 to 2023
$10.9M
Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
NCI NIH HHS CA092900NCI NIH HHS P01 CA165997NCI NIH HHS R01 CA092900
6 · The paper itself

Abstract

The major known function of cytokines that belong to type I interferons (IFN, including IFNα and IFNβ) is to mount the defense against viruses. This function also protects the genetic information of host cells from alterations in the genome elicited by some of these viruses. Furthermore, recent studies demonstrated that IFN also restrict proliferation of damaged cells by inducing cell senescence. Here we investigated the subsequent role of IFN in elimination of the senescent cells. Our studies demonstrate that endogenous IFN produced by already senescent cells contribute to increased expression of the natural killer (NK) receptor ligands, including MIC-A and ULBP2. Furthermore, neutralization of endogenous IFN or genetic ablation of its receptor chain IFNAR1 compromises the recognition of senescent cells and their clearance in vitro and in vivo. We discuss the role of IFN in protecting the multi-cellular host from accumulation of damaged senescent cells and potential significance of this mechanism in human cancers.

Indexed as

Cellular SenescenceAnimalsCells, CulturedFibroblastsGPI-Linked ProteinsHistocompatibility Antigens Class IHumansIntercellular Signaling Peptides and ProteinsInterferon-betaInterferon Type IMice, Inbred C57BLMice, Mutant StrainsNK Cell Lectin-Like Receptor Subfamily KProgeriaReceptor, Interferon alpha-betaWerner SyndromeGPI-Linked ProteinsHistocompatibility Antigens Class IIfnar1 protein, mouseIntercellular Signaling Peptides and ProteinsInterferon-betaInterferon Type IKLRK1 protein, humanMHC class I-related chain ANK Cell Lectin-Like Receptor Subfamily KReceptor, Interferon alpha-betaULBP2 protein, humanDDR, DNA damage responseHGPS, Hutchinson-Gilford progeria syndromeIFNAR1, type I IFN receptorIFN, type I interferonsinterferonNK cellsNK, natural killer cellsSA-βGal, senescence-associated β-galactosidasesenescencesenescent cell clearanceWS, Werner syndrome

Identifiers

PMID26046815
PMCPMC4622626
OpenAlexW1643050643

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.