ArticleMolecular biology of the cell2012
Nucleolar AATF regulates c-Jun-mediated apoptosis.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- AATF supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an NRF-1-dependent mechanism.Cell death & disease · 2026Article
- Network pharmacology study to explore the multiple molecular mechanism of SH003 in the treatment of non-small cell lung cancer.BMC complementary medicine and therapies · 2024Article
- Augmenting MEK inhibitor efficacy in BRAF wild-type melanoma: synergistic effects of disulfiram combination therapy.Journal of experimental & clinical cancer research : CR · 2024Article
- AATF/Che-1 localizes to paraspeckles and suppresses R-loops accumulation and interferon activation in Multiple Myeloma.The EMBO journal · 2022Article
- Identification of the Potential Molecular Mechanisms Linking RUNX1 Activity with Nonalcoholic Fatty Liver Disease, by Means of Systems Biology.Biomedicines · 2022Article
- Che-1/AATF binds to RNA polymerase I machinery and sustains ribosomal RNA gene transcription.Nucleic acids research · 2020Article
- AATF/Che-1-An RNA Binding Protein at the Nexus of DNA Damage Response and Ribosome Biogenesis.Frontiers in oncology · 2020Review
- A protein-RNA interaction atlas of the ribosome biogenesis factor AATF.Scientific reports · 2019Article
- Proteomic Analysis of Breast Cancer Resistance to the Anticancer Drug RH1 Reveals the Importance of Cancer Stem Cells.Cancers · 2019Article
- MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.Apoptosis : an international journal on programmed cell death · 2019Article
- Deacetylation of NAT10 by Sirt1 promotes the transition from rRNA biogenesis to autophagy upon energy stress.Nucleic acids research · 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
- Mitotic cell death caused by follistatin-like 1 inhibition is associated with up-regulated Bim by inactivated Erk1/2 in human lung cancer cells.Oncotarget · 2016Article
- Che-1/AATF: A Critical Cofactor for Both Wild-Type- and Mutant-p53 Proteins.Frontiers in oncology · 2016Review
- Discovering Che-1/AATF: a new attractive target for cancer therapy.Frontiers in genetics · 2015Review
- Identification of protein interactions involved in cellular signaling.Molecular & cellular proteomics : MCP · 2013Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AP-1 transcription factor c-Jun has been shown to be essential for stress-induced apoptosis in several models. However, the molecular mechanisms underlying the proapoptotic activity of c-Jun are poorly understood. We identify the apoptosis-antagonizing transcription factor (AATF) as a novel nucleolar stress sensor, which is required as a cofactor for c-Jun-mediated apoptosis. Overexpression or down-regulation of AATF expression levels led to a respective increase or decrease in the amount of activated and phosphorylated c-Jun with a proportional alteration in the induction levels of the proapoptotic c-Jun target genes FasL and TNF-α. Accordingly, AATF promoted commitment of ultraviolet (UV)-irradiated cells to c-Jun-dependent apoptosis. Whereas AATF overexpression potentiated UV-induced apoptosis in wild-type cells, c-Jun-deficient mouse embryonic fibroblasts were resistant to AATF-mediated apoptosis induction. Furthermore, AATF mutants defective in c-Jun binding were also defective in inducing AP-1 activity and c-Jun-mediated apoptosis. UV irradiation induced a translocation of AATF from the nucleolus to the nucleus, thereby enabling its physical association to c-Jun. Analysis of AATF deletion mutants revealed that the AATF domains required for compartmentalization, c-Jun binding, and enhancement of c-Jun transcriptional activity were all also required to induce c-Jun-dependent apoptosis. These results identify AATF as a nucleolar-confined c-Jun cofactor whose expression levels and spatial distribution determine the stress-induced activity of c-Jun and the levels of c-Jun-mediated apoptosis.
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