ArticleMolecular cell2009
GAMT, a p53-inducible modulator of apoptosis, is critical for the adaptive response to nutrient stress.
Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 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
47 citing papers in PubMed, 90 citations in OpenAlex.
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- Article
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- Prognostic Score Model Based on Ten Differentially Methylated Genes for Predicting Clinical Outcomes in Patients with Adenocarcinoma of the Colon.Cancer management and research · 2021Article
- Metabolic functions of the tumor suppressor p53: Implications in normal physiology, metabolic disorders, and cancer.Molecular metabolism · 2020Review
- Drugging in the absence of p53.Journal of molecular cell biology · 2019Review
- Global miRNA, lncRNA, and mRNA Transcriptome Profiling of Endometrial Epithelial Cells Reveals Genes Related to Porcine Reproductive Failure Caused by Porcine Reproductive and Respiratory Syndrome Virus.Frontiers in immunology · 2019Article
- Exploiting the p53 Pathway for Therapy.Cold Spring Harbor perspectives in medicine · 2017Review
- Predictive significance of HMGCS2 for prognosis in resected Chinese esophageal squamous cell carcinoma patients.OncoTargets and therapy · 2017Article
- Is p53 Involved in Tissue-Specific Insulin Resistance Formation?Oxidative medicine and cellular longevity · 2017Review
- The role of the p53 tumor suppressor in metabolism and diabetes.The Journal of endocrinology · 2016Review
- From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence.Cell metabolism · 2016Review
- SCO2 Mediates Oxidative Stress-Induced Glycolysis to Oxidative Phosphorylation Switch in Hematopoietic Stem Cells.Stem cells (Dayton, Ohio) · 2016Article
- Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation.Cell cycle (Georgetown, Tex.) · 2015Article
- Two-way communication between the metabolic and cell cycle machineries: the molecular basis.Cell cycle (Georgetown, Tex.) · 2015Review
- Essential versus accessory aspects of cell death: recommendations of the NCCD 2015.Cell death and differentiation · 2015Review
- New insights into p53 functions through its target microRNAs.Journal of molecular cell biology · 2014Review
- Regulation of cancer metabolism by O-GlcNAcylation.Glycoconjugate journal · 2014Review
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Creatine transporter (SLC6A8) knockout mice display an increased capacity for in vitro creatine biosynthesis in skeletal muscle.Frontiers in physiology · 2014Article
Corrections and comments
- Retraction · 2013-08-22Duplication of/in Image · Error in Image · Unreliable Results and/or Conclusions ·
- Commented on by
- Retracted
Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
The p53 tumor suppressor protein has a well-established role in cell-fate decision-making processes. However, recent discoveries indicate that p53 has a non-tumor-suppressive role. Here we identify guanidinoacetate methyltransferase (GAMT), an enzyme involved in creatine synthesis, as a p53 target gene and a key downstream effector of adaptive response to nutrient stress. We show that GAMT is not only involved in p53-dependent apoptosis in response to genotoxic stress but is important for apoptosis induced by glucose deprivation. Additionally, p53-->GAMT upregulates fatty acid oxidation (FAO) induced by glucose starvation, utilizing this pathway as an alternate ATP-generating energy source. These results highlight that p53-dependent regulation of GAMT allows cells to maintain energy levels sufficient to undergo apoptosis or survival under conditions of nutrient stress. The p53-->GAMT pathway represents a new link between cellular stress responses and processes of creatine synthesis and FAO, demonstrating a further role of p53 in cellular metabolism.
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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.