Evidence map›Paper›PMID 35138119›Full record

ArticleMicrobiology spectrum2022

The Interferon-Inducible Human PLSCR1 Protein Is a Restriction Factor of Human Cytomegalovirus.

Hidetaka Sadanari, Masaya Takemoto, Tomoki Ishida, Hikaru Otagiri, Tohru Daikoku, Tsugiya Murayama, Shuichi Kusano

Open access · goldAbstract read
In one paragraph

Article in Microbiology spectrum, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Plscr1 inhibits murine norovirus entry.bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Article
  4. IFN-inducible human phospholipid scramblase 1 (PLSCR1) protein restricts HIV-1 infection by inhibiting membrane fusion.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Phospholipid scramblase 1: a frontline defense against viral infections.Frontiers in cellular and infection microbiology · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 2 institutions in 1 country.

Hidetaka Sadanari *Department of Pharmaceutical Life Sciences, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Masaya TakemotoResearch Center for Pharmaceutical Education, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Tomoki IshidaDepartment of Pharmaceutical Life Sciences, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Hikaru OtagiriDepartment of Pharmaceutical Life Sciences, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Tohru DaikokuDepartment of Pharmaceutical Life Sciences, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Tsugiya MurayamaDepartment of Pharmaceutical Life Sciences, Faculty of Pharmaceutical Sciences, Hokuriku Universitygrid.412171.0, Ishikawa, Japan.
Shuichi Kusano *Division of Biological Information Technology, Joint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima, Japan.ORCID 0000-0001-6293-486X
Hokuriku University · JPKagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human phospholipid scramblase 1 (PLSCR1) is strongly expressed in response to interferon (IFN) treatment and viral infection, and it has been suggested to play an important role in IFN-dependent antiviral responses. In this study, we showed that the levels of human cytomegalovirus (HCMV) plaque formation in OUMS-36T-3 (36T-3) cells with high basal expression of PLSCR1 were significantly lower than those in human embryonic lung (HEL) cells with low basal expression of PLSCR1. In addition, the levels of HCMV plaque formation and replication in PLSCR1-knockout (KO) 36T-3 cells were significantly higher than those in parental 36T-3 cells and were comparable to those in HEL cells. Furthermore, compared to that in PLSCR1-KO cells, the expression of HCMV major immediate early (MIE) proteins was repressed and/or delayed in parental 36T-3 cells after HCMV infection. We also showed that PLSCR1 expression decreased the levels of the cAMP-responsive element (CRE)-binding protein (CREB)•HCMV immediate early protein 2 (IE2) and CREB-binding protein (CBP)•IE2 complexes, which have been suggested to play important roles in the IE2-mediated transactivation of the viral early promoter through interactions with CREB, CBP, and IE2. Interestingly, PLSCR1 expression repressed CRE- and HCMV MIE promoter-regulated reporter gene activities. These observations reveal, for the first time, that PLSCR1 negatively regulates HCMV replication by repressing the transcription from viral MIE and early promoters, and that PLSCR1 expression may contribute to the IFN-mediated suppression of HCMV infection.

Indexed as

Antigens, ViralCREB-Binding ProteinCytomegalovirusCytomegalovirus InfectionsGene Expression Regulation, ViralHost-Pathogen InteractionsHumansImmediate-Early ProteinsInterferonsPhospholipid Transfer ProteinsVirus ReplicationAntigens, ViralCREB-Binding ProteinCREBBP protein, humanImmediate-Early Proteinsimmediate-early proteins, cytomegalovirusInterferonsPhospholipid Transfer ProteinsPLSCR1 protein, humangenome editinghuman cytomegalovirusinterferon-stimulated genesphospholipid scramblase 1protein-protein interactionsrestriction factors

Identifiers

PMID35138119
PMCPMC8826943
OpenAlexW4210917133

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.