ArticleCell cycle (Georgetown, Tex.)2013
GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 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
54 citing papers in PubMed, 88 citations in OpenAlex.
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- Glutaminase inhibition as potential cancer therapeutics: current status and future applications.Journal of enzyme inhibition and medicinal chemistry · 2024Review
- TAp73 regulates mitochondrial dynamics and multiciliated cell homeostasis through an OPA1 axis.Cell death & disease · 2024Article
- Glutamine and leukemia research: progress and clinical prospects.Discover oncology · 2024Review
- Prostate Cancer's Silent Partners: Fibroblasts and Their Influence on Glutamine Metabolism Manipulation.International journal of molecular sciences · 2024Article
- Glucose-derived glutamate drives neuronal terminal differentiation in vitro.EMBO reports · 2024Article
- Glutamine addiction in tumor cell: oncogene regulation and clinical treatment.Cell communication and signaling : CCS · 2024Review
- Inhibition of glutaminase-1 in DLBCL potentiates venetoclax-induced antitumor activity by promoting oxidative stress.Blood advances · 2023Article
- Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023Review
- Pathological implications of metabolic reprogramming and its therapeutic potential in medulloblastoma.Frontiers in cell and developmental biology · 2022Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Understanding p53 tumour suppressor network.Biology direct · 2021Article
- Review
- CRISPR-Mediated Induction of Neuron-Enriched Mitochondrial Proteins Boosts Direct Glia-to-Neuron Conversion.Cell stem cell · 2021Article
- Expression ofJournal of ophthalmology · 2021Article
- The Synthetic Cannabinoids THJ-2201 and 5F-PB22 Enhance In Vitro CBInternational journal of molecular sciences · 2020Article
- P73 C-terminus is dispensable for multiciliogenesis.Cell cycle (Georgetown, Tex.) · 2020Article
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Targeting Glutaminolysis: New Perspectives to Understand Cancer Development and Novel Strategies for Potential Target Therapies.Frontiers in oncology · 2020Review
- The Epithelial to Mesenchymal Transition Promotes Glutamine Independence by SuppressingCancers · 2019Article
Corrections and comments
- Commented on by
- Commented on by
- Erratum issued
Authors and funding
11 authors at 8 institutions in 7 countries.
Funding
Abstract
The amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). Two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53. Here, we show that the p53 family member TAp73 also drives the expression of GLS2. Specifically, we demonstrate that TAp73 regulates GLS2 during retinoic acid-induced terminal neuronal differentiation of neuroblastoma cells, and overexpression or inhibition of GLS2 modulates neuronal differentiation and intracellular levels of ATP. Moreover, inhibition of GLS activity, by removing Glutamine from the growth medium, impairs in vitro differentiation of cortical neurons. Finally, expression of GLS2 increases during mouse cerebellar development. Although, p73 is dispensable for the in vivo expression of GLS2, TAp73 loss affects GABA and Glutamate levels in cortical neurons. Together, these findings suggest a role for GLS2 acting, at least in part, downstream of p73 in neuronal differentiation and highlight a possible role of p73 in regulating neurotransmitter synthesis.
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.