ReviewFrontiers in oncology2016
Che-1/AATF: A Critical Cofactor for Both Wild-Type- and Mutant-p53 Proteins.
Review in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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
16 citing papers in PubMed, 26 citations in OpenAlex.
- AATF supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an NRF-1-dependent mechanism.Cell death & disease · 2026Article
- Monocytic Differentiation of Human Acute Myeloid Leukemia Cells: A Proteomic and Phosphoproteomic Comparison of FAB-M4/M5 Patients with and without Nucleophosmin 1 Mutations.International journal of molecular sciences · 2024Article
- The Oncogenic and Immunological Roles of Apoptosis Antagonistic Transcription Factors in Human Tumors: A Pan-Cancer Analysis.Oxidative medicine and cellular longevity · 2022Article
- CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.Journal of experimental & clinical cancer research : CR · 2021Article
- Apoptosis-antagonizing transcription factor is involved in rat post-traumatic epilepsy pathogenesis.Experimental and therapeutic medicine · 2021Article
- AATF is Overexpressed in Human Bladder Cancer and Regulates Chemo-Sensitivity Through Survivin.OncoTargets and therapy · 2021Article
- AATF and SMARCA2 are associated with thyroid volume in Hashimoto's thyroiditis patients.Scientific reports · 2020Article
- A protein-RNA interaction atlas of the ribosome biogenesis factor AATF.Scientific reports · 2019Article
- MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.Apoptosis : an international journal on programmed cell death · 2019Article
- The PI3K/AKT axis modulates AATF activity in Wilms' tumor cells.FEBS open bio · 2018Article
- Che-1 is targeted by c-Myc to sustain proliferation in pre-B-cell acute lymphoblastic leukemia.EMBO reports · 2018Article
- AATF suppresses apoptosis, promotes proliferation and is critical for Kras-driven lung cancer.Oncogene · 2018Article
- p53 is required for brain growth but is dispensable for resistance to nutrient restriction during Drosophila larval development.PloS one · 2018Article
- Che1/AATF interacts with subunits of the histone acetyltransferase core module of SAGA complexes.PloS one · 2017Article
- Human AATF/Che-1 forms a nucleolar protein complex with NGDN and NOL10 required for 40S ribosomal subunit synthesis.Nucleic acids research · 2016Article
- eEF1Bγ binds the Che-1 and TP53 gene promoters and their transcripts.Journal of experimental & clinical cancer research : CR · 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 protein is a key player in a wide range of protein networks that allow the state of "good health" of the cell. Not surprisingly, mutations of the TP53 gene are one of the most common alterations associated to cancer cells. Mutated forms of p53 (mtp53) not only lose the ability to protect the integrity of the genetic heritage of the cell but also acquire pro-oncogenic functions, behaving like dangerous accelerators of transformation and tumor progression. In recent years, many studies focused on investigating possible strategies aiming to counteract this mutant p53 "gain of function" but the results have not always been satisfactory. Che-1/AATF is a nuclear protein that binds to RNA polymerase II and plays a role in multiple fundamental processes, including control of transcription, cell cycle regulation, DNA damage response, and apoptosis. Several studies showed Che-1/AATF as an important endogenous regulator of p53 expression and activity in a variety of biological processes. Notably, this same regulation was more recently observed also on mtp53. The depletion of Che-1/AATF strongly reduces the expression of mutant p53 in several tumors in vitro and in vivo, making the cells an easier target for chemotherapy treatments. In this mini review, we report an overview of Che-1/AATF functions and discuss a possible role of Che-1/AATF in cancer therapy, with particular regard to its action on p53/mtp53.
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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.