ArticlePloS one2015
GIMAP5 Deficiency Is Associated with Increased AKT Activity in T Lymphocytes.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Unexpected genetically determined immune dysregulation with liver involvement: GIMAP5 therapeutic dilemmas between targeted therapy and HSCT.Frontiers in immunology · 2026Article
- Multi-omic analysis of PBMCs in sepsis reveals widespread cytotoxic dysfunction and an increased population ofFrontiers in immunology · 2025Article
- GIMAP5 deficiency reveals a mammalian ceramide-driven longevity assurance pathway.Nature immunology · 2024Article
- Essential role of MFSD1-GLMP-GIMAP5 in lymphocyte survival and liver homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The GIMAP Family Proteins: An Incomplete Puzzle.Frontiers in immunology · 2021Review
- Article
- GTPase of the Immune-Associated Nucleotide Protein 5 Regulates the Lysosomal Calcium Compartment in T Lymphocytes.Frontiers in immunology · 2017Article
- Article
- TCR and IL-7 Signaling Are Altered in the Absence of Functional GTPase of the Immune Associated Nucleotide Binding Protein 5 (GIMAP5).PloS one · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Long-term survival of T lymphocytes in quiescent state is essential to maintain their cell numbers in secondary lymphoid organs. In mice and in rats, the loss of functional GTPase of the immune associated nucleotide binding protein 5 (GIMAP5) causes peripheral T lymphopenia due to spontaneous death of T cells. The underlying mechanism responsible for the disruption of quiescence in Gimap5 deficient T cells remains largely unknown. In this study, we show that loss of functional Gimap5 results in increased basal activation of mammalian target of rapamycin (mTOR), independent of protein phosphatase 2A (PP2A) or AMP-activated protein kinase (AMPK). Our results suggest that the constitutive activation of the phosphoinositide 3-kinase (PI3K) pathway may be one of the consequences of the absence of functional GIMAP5.
Indexed as
Identifiers
What OpenQuestion holds
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.