Evidence map›Paper›PMID 25716322›Full record

ArticleThe Journal of biological chemistry2015

Type I interferon controls propagation of long interspersed element-1.

Qiujing Yu, Christopher J Carbone, Yuliya V Katlinskaya, Hui Zheng, Ke Zheng, Mengcheng Luo, P Jeremy Wang, Roger A Greenberg, Serge Y Fuchs

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-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

45 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
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  3. BeyondInternational journal of molecular sciences · 2025
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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

9 authors at 3 institutions in 3 countries.

Qiujing YuFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Christopher J CarboneFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Yuliya V KatlinskayaFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Hui ZhengFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Ke ZhengFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Mengcheng LuoFrom the Departments of Animal Biology, School of Veterinary Medicine and.
P Jeremy WangFrom the Departments of Animal Biology, School of Veterinary Medicine and.
Roger A GreenbergCancer Biology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Serge Y FuchsFrom the Departments of Animal Biology, School of Veterinary Medicine and syfuchs@vet.upenn.edu.
University of Veterinary and Animal Sciences · PKParker Institute for Cancer Immunotherapy · USSylhet Agricultural University · BD

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
Interferon Responses in Myeloid LeukemiaR01CA142425 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2010 to 2014
$1.6M
NCI NIH HHS CA092900NCI NIH HHS CA142425NCI NIH HHS P01 CA165997NCI NIH HHS R01 CA092900NCI NIH HHS R01 CA142425
6 · The paper itself

Abstract

Type I interferons (IFN) including IFNα and IFNβ are critical for the cellular defense against viruses. Here we report that increased levels of IFNβ were found in testes from mice deficient in MOV10L1, a germ cell-specific RNA helicase that plays a key role in limiting the propagation of retrotransposons including Long Interspersed Element-1 (LINE-1). Additional experiments revealed that activation of LINE-1 retrotransposons increases the expression of IFNβ and of IFN-stimulated genes. Conversely, pretreatment of cells with IFN suppressed the replication of LINE-1. Furthermore, the efficacy of LINE-1 replication was increased in isogenic cell lines harboring inactivating mutations in diverse elements of the IFN signaling pathway. Knockdown of the IFN receptor chain IFNAR1 also stimulated LINE-1 propagation in vitro. Finally, a greater accumulation of LINE-1 was found in mice that lack IFNAR1 compared with wild type mice. We propose that LINE-1-induced IFN plays an important role in restricting LINE-1 propagation and discuss the putative role of IFN in preserving the genome stability.

Indexed as

Long Interspersed Nucleotide ElementsAnimalsEmbryo, MammalianFibroblastsGene Expression RegulationGenomic InstabilityHeLa CellsHumansInterferon-alphaInterferon-betaMaleMiceMice, Inbred C57BLMice, KnockoutNIH 3T3 CellsPrimary Cell CultureIfnar1 protein, mouseInterferon-alphaInterferon-betaMov10l1 protein, mouseReceptor, Interferon alpha-betaRNA HelicasesDNA damagegenomic instabilityinterferonLINE-1radiationreceptorretrotransposonsignaling

Identifiers

PMID25716322
PMCPMC4400334
OpenAlexW2057619489

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.