ArticleNature2016
Metabolic maintenance of cell asymmetry following division in activated T lymphocytes.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 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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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.
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Who cites it
172 citing papers in PubMed, 269 citations in OpenAlex.
- Fate induction through asymmetric T cell division is modulated by chimeric antigen receptor costimulatory domains.Nature immunology · 2026Article
- Single-cell gain-of-function mapping reveals latent regulatory programs governing CD8Research square · 2026Article
- An early burst of cytokine production before the first cell division influences CD8 T cell differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mitochondrial asymmetry shifts T cell fate.Nature cell biology · 2026Article
- Autophagy-regulated mitochondrial inheritance controls early CD8Nature cell biology · 2026Article
- Glycolysis maintains effector function of lung Th17 TRM cells in precision cut lung slices.iScience · 2025Article
- Dysfunctional mitochondria in ageing T cells: a perspective on mitochondrial quality control mechanisms.EMBO reports · 2025Review
- A Dapl1Science advances · 2025Article
- CCR2Cellular & molecular immunology · 2025Article
- Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging.npj aging · 2025Review
- Immune regeneration: implications for cancer immunotherapy and beyond.The Journal of clinical investigation · 2025Review
- Epigenetic Regulation of CD8European journal of immunology · 2025Article
- Lysosomal NKG7 restrains mTORC1 activity to promote CD8Nature communications · 2025Article
- MYO1F regulates T-cell activation and glycolytic metabolism by promoting the acetylation of GAPDH.Cellular & molecular immunology · 2025Article
- Metabolic reprogramming of CAR T cells: a new frontier in cancer immunotherapy.Frontiers in immunology · 2025Review
- Deciphering the deterministic role of TCR signaling in T cell fate determination.Frontiers in immunology · 2025Review
- Integrative analysis of polyamine metabolism-related genes in gliomas: implications for prognosis and therapy.Frontiers in oncology · 2025Article
- Acidity suppresses CD8 + T-cell function by perturbing IL-2, mTORC1, and c-Myc signaling.The EMBO journal · 2024Article
- Double-Faced Immunological Effects of CDK4/6 Inhibitors on Cancer Treatment: Challenges and Perspectives.Bioengineering (Basel, Switzerland) · 2024Review
- Article
112 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Asymmetric cell division, the partitioning of cellular components in response to polarizing cues during mitosis, has roles in differentiation and development. It is important for the self-renewal of fertilized zygotes in Caenorhabditis elegans and neuroblasts in Drosophila, and in the development of mammalian nervous and digestive systems. T lymphocytes, upon activation by antigen-presenting cells (APCs), can undergo asymmetric cell division, wherein the daughter cell proximal to the APC is more likely to differentiate into an effector-like T cell and the distal daughter is more likely to differentiate into a memory-like T cell. Upon activation and before cell division, expression of the transcription factor c-Myc drives metabolic reprogramming, necessary for the subsequent proliferative burst. Here we find that during the first division of an activated T cell in mice, c-Myc can sort asymmetrically. Asymmetric distribution of amino acid transporters, amino acid content, and activity of mammalian target of rapamycin complex 1 (mTORC1) is correlated with c-Myc expression, and both amino acids and mTORC1 activity sustain the differences in c-Myc expression in one daughter cell compared to the other. Asymmetric c-Myc levels in daughter T cells affect proliferation, metabolism, and differentiation, and these effects are altered by experimental manipulation of mTORC1 activity or c-Myc expression. Therefore, metabolic signalling pathways cooperate with transcription programs to maintain differential cell fates following asymmetric T-cell division.
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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.