ArticleCell death and differentiation2011
NF-Y is essential for expression of the proapoptotic bim gene in sympathetic neurons.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- NFYA regulates two sequential genome-wide transcriptional activation events during oocyte to embryo transition.bioRxiv : the preprint server for biology · 2026Article
- Cracking the Code of Neuronal Cell Fate.Cells · 2023Review
- BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023Review
- An Excess of CYP24A1, Lack of CaSR, and a Novel lncRNA Near the PTH Gene Characterize an Ectopic PTH-Producing Tumor.Journal of the Endocrine Society · 2017Article
- Loss of GCN5 leads to increased neuronal apoptosis by upregulating E2F1- and Egr-1-dependent BH3-only protein Bim.Cell death & disease · 2017Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1.Nucleic acids research · 2014Article
- Programmed cell death during neuronal development: the sympathetic neuron model.Cell death and differentiation · 2014Review
- Upregulated expression of NF-YC contributes to neuronal apoptosis via proapoptotic protein bim in rats' brain hippocampus following middle cerebral artery occlusion (MCAO).Journal of molecular neuroscience : MN · 2014Article
- A feed-forward loop involving Trib3, Akt and FoxO mediates death of NGF-deprived neurons.Cell death and differentiation · 2013Article
- Caspase-2 is essential for c-Jun transcriptional activation and Bim induction in neuron death.The Biochemical journal · 2013Article
- NF-Y coassociates with FOS at promoters, enhancers, repetitive elements, and inactive chromatin regions, and is stereo-positioned with growth-controlling transcription factors.Genome research · 2013Article
- NF-YA underlies EZH2 upregulation and is essential for proliferation of human epithelial ovarian cancer cells.Molecular cancer research : MCR · 2013Article
- Gene-specific factors determine mitotic expression and bookmarking via alternate regulatory elements.Nucleic acids research · 2013Article
- Review
- Arsenic trioxide-induced growth arrest of breast cancer MCF-7 cells involving FOXO3a and IκB kinase β expression and localization.Cancer biotherapy & radiopharmaceuticals · 2012Article
- Global analysis of gene expression in NGF-deprived sympathetic neurons identifies molecular pathways associated with cell death.BMC genomics · 2011Article
- The MEK-ERK pathway negatively regulates bim expression through the 3' UTR in sympathetic neurons.BMC neuroscience · 2011Article
- NF-Y joins E2Fs, p53 and other stress transcription factors at the apoptosis table.Cell death & disease · 2011Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Neuronal apoptosis has a major role during development and aberrant apoptosis contributes to the pathology of certain neurological conditions. Studies with nerve growth factor (NGF)-dependent sympathetic neurons have provided important insights into the molecular mechanisms of neuronal apoptosis and the signalling pathways that regulate the cell death programme in neurons. The BH3-only protein Bim is a critical mediator of apoptosis in many cell types and in sympathetic neurons is required for NGF withdrawal-induced death. However, regulation of bim expression is complex and remains incompletely understood. We report that a conserved inverted CCAAT box (ICB) in the rat bim promoter is bound by the heterotrimeric transcription factor NF-Y. Interestingly, NF-Y is required for bim promoter activity and its induction following NGF withdrawal. We demonstrate that NF-Y activity is essential for endogenous Bim expression and contributes to NGF withdrawal-induced death. Furthermore, we find that the transcriptional coactivators CBP and p300 interact with NF-Y and FOXO3a and bind to this region of the bim promoter. The amount of CBP/p300 bound to bim increases after NGF deprivation and inhibition of CBP/p300 activity reduces bim induction. Our results indicate that NF-Y cooperates with FOXO3a to recruit CBP/p300 to the bim promoter to form a stable multi-protein/DNA complex that activates bim transcription after survival factor withdrawal.
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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.