ArticleOncotarget2016
Tumor suppressor BTG1 promotes PRMT1-mediated ATF4 function in response to cellular stress.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 39 citations in OpenAlex.
- Tamoxifen for the treatment of myeloproliferative neoplasms: A Phase II clinical trial and exploratory analysis.Nature communications · 2023Trial
- Small-Molecule Activators of PRMT1: Discovery, SAR Analyses, and Proapoptotic Effects in Pancreatic Cancer Cells.Journal of medicinal chemistry · 2026Article
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting the PRMT1 axis in cancer: from epigenetic plasticity to contextual therapeutic interventions.Frontiers in oncology · 2026Review
- PC3/Tis21/BTG2 and BTG1 genes: regulators of the cell cycle and neurogenesis, as well as tumor suppressors in malignant brain tumors.Frontiers in cell and developmental biology · 2026Review
- Insight into the Regulation of NDRG1 Expression.International journal of molecular sciences · 2025Review
- Ferroptosis contributes to immunosuppression.Frontiers of medicine · 2025Review
- Context-dependent roles of mitochondrial LONP1 in orchestrating the balance between airway progenitor versus progeny cells.Cell stem cell · 2024Article
- Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.Research square · 2024Article
- ATF4 in cellular stress, ferroptosis, and cancer.Archives of toxicology · 2024Review
- PRMT1 in human neoplasm: cancer biology and potential therapeutic target.Cell communication and signaling : CCS · 2024Review
- Targeting the PRMT1-cGAS-STING signaling pathway to enhance the anti-tumor therapeutic efficacy.Journal of cancer biology · 2024Article
- Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.Npj biological timing and sleep · 2024Article
- Btg1 and Btg2 regulate neonatal cardiomyocyte cell cycle arrest.Journal of molecular and cellular cardiology · 2023Article
- Signaling plasticity in the integrated stress response.Frontiers in cell and developmental biology · 2023Review
- Emerging role of anti-proliferative protein BTG1 and BTG2.BMB reports · 2022Review
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- A conserved motif in human BTG1 and BTG2 proteins mediates interaction with the poly(A) binding protein PABPC1 to stimulate mRNA deadenylation.RNA biology · 2021Article
- Arginine methylation and ubiquitylation crosstalk controls DNA end-resection and homologous recombination repair.Nature communications · 2021Article
- Inducible Prmt1 ablation in adult vascular smooth muscle leads to contractile dysfunction and aortic dissection.Experimental & molecular medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Cancer cells are frequently exposed to physiological stress conditions such as hypoxia and nutrient limitation. Escape from stress-induced apoptosis is one of the mechanisms used by malignant cells to survive unfavorable conditions. B-cell Translocation Gene 1 (BTG1) is a tumor suppressor that is frequently deleted in acute lymphoblastic leukemia and recurrently mutated in diffuse large B cell lymphoma. Moreover, low BTG1 expression levels have been linked to poor outcome in several solid tumors. How loss of BTG1 function contributes to tumor progression is not well understood. Here, using Btg1 knockout mice, we demonstrate that loss of Btg1 provides a survival advantage to primary mouse embryonic fibroblasts (MEFs) under stress conditions. This pro-survival effect involves regulation of Activating Transcription Factor 4 (ATF4), a key mediator of cellular stress responses. We show that BTG1 interacts with ATF4 and positively modulates its activity by recruiting the protein arginine methyl transferase PRMT1 to methylate ATF4 on arginine residue 239. We further extend these findings to B-cell progenitors, by showing that loss of Btg1 expression enhances stress adaptation of mouse bone marrow-derived B cell progenitors. In conclusion, we have identified the BTG1/PRMT1 complex as a new modifier of ATF4 mediated stress responses.
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.