Evidence map›Paper›PMID 39288763›Full record

ArticleCell genomics2024

Functional and dynamic profiling of transcript isoforms reveals essential roles of alternative splicing in interferon response.

Mahoko Takahashi Ueda, Jun Inamo, Fuyuki Miya, Mihoko Shimada, Kensuke Yamaguchi, Yuta Kochi

Abstract read
In one paragraph

Article in Cell genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Dysregulation of U12-Type Splicing in Lupus Neutrophils.Arthritis & rheumatology (Hoboken, N.J.) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Dysregulation of U12-Type Splicing in Lupus Neutrophils.bioRxiv : the preprint server for biology · 2025
    Article
  14. Review
  15. Review
  16. 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

6 authors.

Mahoko Takahashi UedaDepartment of Genomic Function and Diversity, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Jun InamoDivision of Rheumatology, University of Colorado School of Medicine, Aurora, CO, USA; Department of Biomedical Informatics, Center for Health Artificial Intelligence, University of Colorado School of Medicine, Aurora, CO, USA.
Fuyuki MiyaCenter for Medical Genetics, Keio University School of Medicine, Tokyo 160-8582, Japan.
Mihoko ShimadaNational Center for Global Health and Medicine, Tokyo 162-8655, Japan.
Kensuke YamaguchiBiomedical Engineering Research Innovation Center, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; Laboratory for Autoimmune Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa 230-0045, Japan; Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuta KochiDepartment of Genomic Function and Diversity, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address: y-kochi.gfd@mri.tmd.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon (IFN-I) plays an important role in the innate immune response through inducing IFN-I-stimulated genes (ISGs). However, how alternative splicing (AS) events, especially over time, affect their function remains poorly understood. We generated an annotation (113,843 transcripts) for IFN-I-stimulated human B cells called isoISG using high-accuracy long-read sequencing data from PacBio Sequel II/IIe. Transcript isoform profiling using isoISG revealed that isoform switching occurred in the early response to IFN-I so that ISGs would gain functional domains (e.g., C4B) or higher protein production (e.g., IRF3). Conversely, isoforms lacking functional domains increased during the late phase of IFN-I response, mainly due to intron retention events. This suggests that isoform switching both triggers and terminates IFN-I responses at the translation and protein levels. Furthermore, genetic variants influencing the isoform ratio of ISGs were associated with immunological and infectious diseases. AS has essential roles in regulating innate immune response and associated diseases.

Indexed as

Alternative SplicingProtein IsoformsB-LymphocytesGene Expression ProfilingHumansImmunity, InnateInterferon Type IInterferon Type IProtein Isoformsalternative splicing regulationinterferon-stimulated genesintron retentionISGsisoform switchinglong-read RNA-seqPacBio Sequel II/IIe

Identifiers

PMID39288763
PMCPMC11602592

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.