ReviewNeurochemical research2017
AKT/GSK3β Signaling in Glioblastoma.
Review in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Tracing the origins of glioblastoma by investigating the role of gliogenic and related neurogenic genes/signaling pathways in GBM development: a systematic review.World journal of surgical oncology · 2022Pooled it
- Cistanoside A decreases Tau hyperphosphorylation and neuronal apoptosis through the AKT/GSK3β pathway in okadaic acid-induced in vivo and in vitro models of Alzheimer's disease.Molecular biology reports · 2026Article
- Review
- Review
- Camellia oil supplementation specifically enhances marbling scores via PI3K/Akt pathway while optimizing n-6/n-3 fatty acid ratios: A dual-benefit strategy for premium functional beef production.Food chemistry: X · 2026Article
- SLIT3: a novel regulator of odontogenic differentiation through Akt/GSK3β/β-catenin signaling pathway.International journal of oral science · 2026Article
- MLN4924 inhibits macrophage foam cell formation by enhancing autophagy and regulating metabolic phenotype.Lipids in health and disease · 2025Article
- Recent Advances in Marine-Derived Nanoformulation for the Management of Glioblastoma.Molecular biotechnology · 2025Review
- Natural Metabolites as Modulators of Sensing and Signaling Mechanisms: Unlocking Anti-Ovarian Cancer Potential.Biomedicines · 2025Review
- Article
- AAV-mediated GBA1 and GDNF rescue neurological defects in a murine model of neuronopathic Gaucher disease.Molecular therapy. Nucleic acids · 2025Article
- Molecular targets of vortioxetine mediating glioblastoma suppression revealed by gene and protein network analyses and molecular docking simulations.The international journal of neuropsychopharmacology · 2025Article
- Review
- Mechanistic Insights into the Anti-Glioma Effects of Exosome-Like Nanoparticles Derived fromInternational journal of nanomedicine · 2025Article
- Exploring glioma heterogeneity through omics networks: from gene network discovery to causal insights and patient stratification.BioData mining · 2024Article
- S-acylation of CaChronic diseases and translational medicine · 2024Review
- Unraveling the role of LncRNAs in glioblastoma progression: insights into signaling pathways and therapeutic potential.Metabolic brain disease · 2024Review
- Chlorogenic Acid and Cinnamaldehyde in Combination Inhibit Metastatic Traits and Induce Apoptosis via Akt Downregulation in Breast Cancer Cells.International journal of molecular sciences · 2024Article
- VEGFR2 blockade inhibits glioblastoma cell proliferation by enhancing mitochondrial biogenesis.Journal of translational medicine · 2024Article
- Dietary supplementation with pyrroloquinoline quinone promotes growth, relieves weaning stress, and regulates metabolism of piglets compared with adding zinc oxide.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
12 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM.
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.