ArticleeLife2022
Alternative splicing of apoptosis genes promotes human T cell survival.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Coordination of nuclear RNA processing by speckle-localized kinase TAOK2.Genes & development · 2026Article
- HnRNPA2B1 tunes antimycobacterial immune responses in macrophages through alternative splicing ofInfection and immunity · 2026Article
- T Cell Heterogeneity Shaped by Alternative Splicing Predicts Prognosis in Hepatocellular Carcinoma.Cancer science · 2026Article
- Alternative splicing contributes to plasticity and regulatory divergence in locally adapted house mice from the Americas.Molecular biology and evolution · 2026Article
- Isoforms in action: The impact of transcript diversity in phenotype.Genetics and molecular biology · 2026Article
- Splice Isoforms of the Apoptosis Gene BCL-X Have Opposing Effects in Diabetic Kidney Disease: Potential Treatment Target and Prognostic Value.Journal of diabetes research · 2026Article
- HnRNPA2B1 tunes antimycobacterial immune responses in macrophages through alternative splicing ofbioRxiv : the preprint server for biology · 2025Article
- Alternatively spliced isoforms of IRF7 differentially regulate interferon expression to tune response to viral infection.Cell reports · 2025Article
- Facts and Hopes: Toward the Next Quantum Leap in Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Unveiling alternative splicing dynamics in activated T lymphocytes and their implications for immune checkpoint blockade efficacy.iScience · 2025Article
- Alternative splicing of immune-related genes identifies breast cancer subtypes with differential immune cell infiltration.Genes & diseases · 2025Article
- Mechanistic Insights into Alternative Gene Splicing in Oxidative Stress and Tissue Injury.Antioxidants & redox signaling · 2024Review
- How does caspases regulation play role in cell decisions? apoptosis and beyond.Molecular and cellular biochemistry · 2024Review
- Alternative 3'UTR expression induced by T cell activation is regulated in a temporal and signal dependent manner.Scientific reports · 2024Article
- Alternative splicing of modulatory immune receptors in T lymphocytes: a newly identified and targetable mechanism for anticancer immunotherapy.Frontiers in immunology · 2024Review
- RNA circuits and RNA-binding proteins in T cells.Trends in immunology · 2023Review
- Review
- Molecular and temporal control of restimulation-induced cell death (RICD) in T lymphocytes.Frontiers in cell death · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing occurs in the vast majority of human genes, giving rise to distinct mRNA and protein isoforms. We, and others, have previously identified hundreds of genes that change their isoform expression upon T cell activation via alternative splicing; however, how these changes link activation input with functional output remains largely unknown. Here, we investigate how costimulation of T cells through the CD28 receptor impacts alternative splicing in T cells activated through the T cell receptor (TCR, CD3) and find that while CD28 signaling alone has minimal impact on splicing, it enhances the extent of change for up to 20% of TCR-induced alternative splicing events. Interestingly, a set of CD28-enhanced splicing events occur within genes encoding key components of the apoptotic signaling pathway; namely caspase-9, Bax, and Bim. Using both CRISPR-edited cells and antisense oligos to force expression of specific isoforms, we show for all three of these genes that the isoform induced by CD3/CD28 costimulation promotes resistance to apoptosis, and that changes in all three genes together function combinatorially to further promote cell viability. Finally, we show that the JNK signaling pathway, induced downstream of CD3/CD28 costimulation, is required for each of these splicing events, further highlighting their co-regulation. Together, these findings demonstrate that alternative splicing is a key mechanism by which costimulation of CD28 promotes viability of activated T cells.
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Registered trials
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.