ArticleNature communications2016
Repression of GSK3 restores NK cell cytotoxicity in AML patients.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
71 citing papers in PubMed, 112 citations in OpenAlex.
- Fc-engineered anti-CD33 monoclonal antibody potentiates cytotoxicity of membrane-bound interleukin-21 expanded natural killer cells in acute myeloid leukemia.Cytotherapy · 2020Trial
- Targeting cholesterol-driven immunometabolism in cancer: from molecular circuits to clinical translation.Molecular cancer · 2026Review
- Engineered natural killer cells for cancer therapy.Cancer cell · 2025Review
- Nanomaterials Trigger Functional Anti-Tumoral Responses in Primary Human Immune Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Metabolic checkpoints in immune cell reprogramming: rewiring immunometabolism for cancer therapy.Molecular cancer · 2025Review
- Perturbing LSD1 and WNT rewires transcription to synergistically induce AML differentiation.Nature · 2025Article
- Reply to 'Comment on: Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation'.Cellular & molecular immunology · 2025Article
- NK cell-based immunotherapy strategies for myeloid leukemia.Frontiers in immunology · 2025Review
- Arachidonic acid impairs natural killer cell functions by disrupting signaling pathways driven by activating receptors and reactive oxygen species.Cell communication and signaling : CCS · 2024Article
- BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML.Science translational medicine · 2024Article
- Reprogramming natural killer cells for cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Venetoclax acts as an immunometabolic modulator to potentiate adoptive NK cell immunotherapy against leukemia.Cell reports. Medicine · 2024Article
- Loss of GSK3β in hematopoietic stem cells results in normal hematopoiesis in mice.Blood advances · 2023Article
- A novel NHEJ gene signature based model for risk stratification and prognosis prediction in hepatocellular carcinoma.Cancer cell international · 2023Article
- Natural Killer T and Natural Killer Cell-Based Immunotherapy Strategies Targeting Cancer.Biomolecules · 2023Review
- Article
- Killer instincts: natural killer cells as multifactorial cancer immunotherapy.Frontiers in immunology · 2023Review
- Metabolic regulation of NK cell function: implications for immunotherapy.Immunometabolism (Cobham, Surrey) · 2023Review
- The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.PloS one · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Natural killer cells from acute myeloid leukaemia patients (AML-NK) show a dramatic impairment in cytotoxic activity. The exact reasons for this dysfunction are not fully understood. Here we show that the glycogen synthase kinase beta (GSK3β) expression is elevated in AML-NK cells. Interestingly, GSK3 overexpression in normal NK cells impairs their ability to kill AML cells, while genetic or pharmacological GSK3 inactivation enhances their cytotoxic activity. Mechanistic studies reveal that the increased cytotoxic activity correlates with an increase in AML-NK cell conjugates. GSK3 inhibition promotes the conjugate formation by upregulating LFA expression on NK cells and by inducing ICAM-1 expression on AML cells. The latter is mediated by increased NF-κB activation in response to TNF-α production by NK cells. Finally, GSK3-inhibited NK cells show significant efficacy in human AML mouse models. Overall, our work provides mechanistic insights into the AML-NK dysfunction and a potential NK cell therapy strategy.
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.