ArticleOncogene2012
Regulated ATF5 loss-of-function in adult mice blocks formation and causes regression/eradication of gliomas.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Outer radial glia promotes white matter regeneration after neonatal brain injury.Cell reports. Medicine · 2025Article
- A bird's eye view of mitochondrial unfolded protein response in cancer: mechanisms, progression and further applications.Cell death & disease · 2024Review
- Activating transcription factor 5 (ATF5) controls intestinal tuft and goblet cell expansion upon succinate-induced type 2 immune responses in mice.Cell and tissue research · 2023Article
- Review
- Advancements in Activating Transcription Factor 5 Function in Regulating Cell Stress and Survival.International journal of molecular sciences · 2022Review
- Activating transcription factor 5 (ATF5) promotes tumorigenic capability and activates the Wnt/b-catenin pathway in bladder cancer.Cancer cell international · 2021Article
- Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents.Cancers · 2021Article
- Expression patterns of activating transcription factor 5 (atf5a and atf5b) in zebrafish.Gene expression patterns : GEP · 2020Article
- Dominant-Negative ATF5 Compromises Cancer Cell Survival by Targeting CEBPB and CEBPD.Molecular cancer research : MCR · 2020Article
- Expression of activating transcription factor 5 (ATF5) is mediated by microRNA-520b-3p under diverse cellular stress in cancer cells.PloS one · 2020Article
- Dominant-negative ATF5 rapidly depletes survivin in tumor cells.Cell death & disease · 2019Article
- Metabolic and epigenetic reprogramming in the arsenic-induced cancer stem cells.Seminars in cancer biology · 2019Review
- Expression and targeting of transcription factor ATF5 in dog gliomas.Veterinary and comparative oncology · 2018Article
- A Futile Battle? Protein Quality Control and the Stress of Aging.Developmental cell · 2018Review
- Expression of activating transcription factor 5 (ATF5) is increased in astrocytomas of different WHO grades and correlates with survival of glioblastoma patients.OncoTargets and therapy · 2018Article
- The transcription factor ATF5: role in cellular differentiation, stress responses, and cancer.Oncotarget · 2017Review
- Targeting ATF5 in Cancer.Trends in cancer · 2017Article
- Integrating the UPRCritical reviews in biochemistry and molecular biology · 2017Review
- ATF5 regulates β-cell survival during stress.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastomas are among the most incurable cancers. Our past findings indicated that glioblastoma cells, but not neurons or glia, require the transcription factor ATF5 (activating transcription factor 5) for survival. However, it was unknown whether interference with ATF5 function can prevent or promote regression/eradication of malignant gliomas in vivo. To address this issue, we created a mouse model by crossing a human glial fibrillary acidic protein (GFAP) promoter-tetracycline transactivator mouse line with tetracycline operon-dominant negative-ATF5 (d/n-ATF5) mice to establish bi-transgenic mice. In this model, d/n-ATF5 expression is controlled by doxycycline and the promoter for GFAP, a marker for stem/progenitor cells as well as gliomas. Endogenous gliomas were produced with high efficiency by retroviral delivery of platelet-derived growth factor (PDGF)-B and p53-short hairpin RNA (shRNA) in adult bi-transgenic mice in which expression of d/n-ATF5 was spatially and temporally regulated. Induction of d/n-ATF5 before delivery of PDGF-B/p53-shRNA virus greatly reduced the proportion of mice that formed tumors. Moreover, d/n-ATF5 induction after tumor formation led to regression/eradication of detectable gliomas without evident damage to normal brain cells in all 24 mice assessed.
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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.