Evidence map›Paper›PMID 30682178›Full record

ArticlePLoS pathogens2019

Bclaf1 critically regulates the type I interferon response and is degraded by alphaherpesvirus US3.

Chao Qin, Rui Zhang, Yue Lang, Anwen Shao, Aotian Xu, Wenhai Feng, Jun Han, Mengdong Wang, Wanwei He, Cuilian Yu and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 1 institution in 1 country.

Chao QinState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Rui ZhangState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Yue LangState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Anwen ShaoDepartment of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing, China.
Aotian XuState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Wenhai FengDepartment of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing, China.
Jun HanState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Mengdong WangState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Wanwei HeState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Cuilian YuState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.
Jun TangState Key Laboratory of Agrobiotechnology and College of Veterinary Medicine, China Agricultural University, Beijing, China.ORCID 0000-0002-4540-1647
China Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon response plays a prominent role against viral infection, which is frequently disrupted by viruses. Here, we report Bcl-2 associated transcription factor 1 (Bclaf1) is degraded during the alphaherpesvirus Pseudorabies virus (PRV) and Herpes simplex virus type 1 (HSV-1) infections through the viral protein US3. We further reveal that Bclaf1 functions critically in type I interferon signaling. Knockdown or knockout of Bclaf1 in cells significantly impairs interferon-α (IFNα) -mediated gene transcription and viral inhibition against US3 deficient PRV and HSV-1. Mechanistically, Bclaf1 maintains a mechanism allowing STAT1 and STAT2 to be efficiently phosphorylated in response to IFNα, and more importantly, facilitates IFN-stimulated gene factor 3 (ISGF3) binding with IFN-stimulated response elements (ISRE) for efficient gene transcription by directly interacting with ISRE and STAT2. Our studies establish the importance of Bclaf1 in IFNα-induced antiviral immunity and in the control of viral infections.

Indexed as

AlphaherpesvirinaeAnimalsCell LineChinaHerpesvirus 1, HumanHerpesvirus 1, SuidHumansImmunity, InnateInterferon-alphaInterferonsInterferon-Stimulated Gene Factor 3, alpha SubunitInterferon Type IMiceMice, Inbred BALB CPhosphorylationProtein Serine-Threonine KinasesBCLAF1 protein, humanInterferon-alphaInterferonsInterferon-Stimulated Gene Factor 3, alpha SubunitInterferon Type IProtein Serine-Threonine KinasesRepressor ProteinsSTAT1 Transcription FactorSTAT2 Transcription FactorTumor Suppressor ProteinsUS3 protein, Human herpesvirus 1Viral Proteins

Identifiers

PMID30682178
PMCPMC6364948
OpenAlexW2952818759

What Socratic 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 Socratic graph.