Evidence map›Paper›PMID 34912323›Full record

ArticleFrontiers in microbiology2021

An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells.

Shihao Chen, Ruihan Zhao, Ting Wu, Dedong Wang, Biao Wang, Shiyu Pan, Xuming Hu, Zhiming Pan, Hengmi Cui

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

9 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Functional Bidirectionality of ERV-Derived Long Non-Coding RNAs in Humans.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Advances on genetic and genomic studies of ALV resistance.Journal of animal science and biotechnology · 2022
    Review
  9. 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

9 authors at 1 institution in 1 country.

Shihao ChenInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Ruihan ZhaoInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Ting WuInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Dedong WangInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Biao WangInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Shiyu PanInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Xuming HuInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Zhiming PanJiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou, China.
Hengmi CuiInstitute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Yangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with the avian leukosis virus subgroup J (ALV-J) impairs host genes and facilitates the establishment of chronic infection and the viral life cycle. However, the involvement of long noncoding RNAs (lncRNAs) in ALV-J infection remains largely unknown. In this study, we identified a novel chicken lncRNA derived from LTR5B of the ERV-L family (namely lnc-LTR5B), which is significantly downregulated in ALV-J infected cells. lnc-LTR5B was localized in the cytoplasm and was relatively high expressed in the chicken lung and liver. Notably, the replication of ALV-J was inhibited by the overexpression of lnc-LTR5B but enhanced when lnc-LTR5B expression was knocked down. We further confirmed that lnc-LTR5B could bind to the binding immunoglobulin protein (BiP), a master regulator of endoplasmic reticulum (ER) function. Mechanistically, lnc-LTR5B serves as a competing endogenous RNA for BiP, restricting its physical availability. Upon ALV-J infection, the reduction of lnc-LTR5B released BiP, which facilitated its translocation to the cell surface. This is crucial for ALV-J entry as well as pro-survival signaling. In conclusion, we identified an endogenous retroviral LTR-activated lnc-LTR5B that is involved in regulating the cell surface translocation of BiP, and such regulatory machinery can be exploited by ALV-J to complete its life cycle and propagate.

Indexed as

ALV-JBiPinteractionlnc-LTR5BlncRNA

Identifiers

PMID34912323
PMCPMC8667585
OpenAlexW3216784223

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.