ArticleCell death & disease2016
Kinase-independent function of RIP1, critical for mature T-cell survival and proliferation.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells.Cell death and differentiation · 2026Article
- Ndrg3 is a critical regulator of peripheral T cell maturation and homeostasis.Science advances · 2025Article
- RIPK1 protects naive and regulatory T cells from TNFR1-induced apoptosis.Cell death and differentiation · 2024Article
- Not to be and how not to be: the questions of Tregs controlled by RIPK1.Cellular & molecular immunology · 2024Article
- RIPK1 plays a crucial role in maintaining regulatory T-Cell homeostasis by inhibiting both RIPK3- and FADD-mediated cell death.Cellular & molecular immunology · 2024Article
- Excessive apoptosis of Rip1-deficient T cells leads to premature aging.EMBO reports · 2023Article
- RIPK3 controls MAIT cell accumulation during development but not during infection.Cell death & disease · 2023Article
- RIPK1 blocks T cell senescence mediated by RIPK3 and caspase-8.Science advances · 2023Article
- RIPK1 deficiency prevents thymic NK1.1 expression and subsequent iNKT cell development.Frontiers in immunology · 2023Article
- The scaffold-dependent function of RIPK1 in dendritic cells promotes injury-induced colitis.Mucosal immunology · 2022Article
- Receptor Interacting Protein Kinase Pathways Regulate Innate B Cell Developmental Checkpoints But Not Effector Function in Mice.Frontiers in immunology · 2021Article
- Dysregulation of Cell Death in Human Chronic Inflammation.Cold Spring Harbor perspectives in biology · 2020Review
- RIPK1 can mediate apoptosis in addition to necroptosis during embryonic development.Cell death & disease · 2019Article
- TRADD regulates perinatal development and adulthood survival in mice lacking RIPK1 and RIPK3.Nature communications · 2019Article
- Human RIPK1 deficiency causes combined immunodeficiency and inflammatory bowel diseases.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Radiosynthesis and characterization of a carbon-11 PET tracer for receptor-interacting protein kinase 1.Nuclear medicine and biologyArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The death receptor, Fas, triggers apoptotic death and is essential for maintaining homeostasis in the peripheral lymphoid organs. RIP1 was originally cloned when searching for Fas-binding proteins and was later shown to associate also with the signaling complex of TNFR1. Although Fas exclusively induces apoptosis, TNFR1 primarily activates the pro-survival/pro-inflammatory NF-κB pathway. Mutations in Fas lead to lymphoproliferative (lpr) diseases, and deletion of TNFR1 results in defective innate immune responses. However, the function of RIP1 in the adult lymphoid system has not been well understood, primarily owing to perinatal lethality in mice lacking the entire RIP1 protein in germ cells. This current study investigated the requirement for RIP1 in the T lineage using viable RIP1 mutant mice containing a conditional and kinase-dead RIP1 allele. Disabling the kinase activity of RIP1 had no obvious impact on the T-cell compartment. However, T-cell-specific deletion of RIP1 led to a severe T-lymphopenic condition, owing to a dramatically reduced mature T-cell pool in the periphery. Interestingly, the immature T-cell compartment in the thymus appeared intact. Further analysis showed that mature RIP1
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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.