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Functional and dynamic profiling of transcript isoforms reveals essential roles of alternative splicing in interferon response.
Ueda, Mahoko Takahashi; Inamo, Jun; Miya, Fuyuki; Shimada, Mihoko; Yamaguchi, Kensuke; Kochi, Yuta.
Afiliación
  • Ueda MT; Department of Genomic Function and Diversity, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
  • Inamo J; Division 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.
  • Miya F; Center for Medical Genetics, Keio University School of Medicine, Tokyo 160-8582, Japan.
  • Shimada M; National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
  • Yamaguchi K; Biomedical 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 an
  • Kochi Y; Department 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.
Cell Genom ; 4(10): 100654, 2024 Oct 09.
Article en En | MEDLINE | ID: mdl-39288763
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Empalme Alternativo / Isoformas de Proteínas Límite: Humans Idioma: En Revista: Cell Genom Año: 2024 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
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XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Empalme Alternativo / Isoformas de Proteínas Límite: Humans Idioma: En Revista: Cell Genom Año: 2024 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos