ArticleNucleic acids research2009
The proapoptotic dp5 gene is a direct target of the MLK-JNK-c-Jun pathway in sympathetic neurons.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
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- Genetic architectures of the human hippocampus and those involved in neuropsychiatric traits.BMC medicine · 2024Article
- Cross-ancestry genome-wide association meta-analyses of hippocampal and subfield volumes.Nature genetics · 2023Article
- The Jun-dependent axon regeneration gene program: Jun promotes regeneration over plasticity.Human molecular genetics · 2022Article
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- A novel endoplasmic stress mediator, Kelch domain containing 7B (KLHDC7B), increased Harakiri (HRK) in the SubAB-induced apoptosis signaling pathway.Cell death discovery · 2021Article
- Aberration of the modulatory functions of intronic microRNA hsa-miR-933 on its host gene ATF2 results in type II diabetes mellitus and neurodegenerative disease development.Human genomics · 2020Article
- KAT3-dependent acetylation of cell type-specific genes maintains neuronal identity in the adult mouse brain.Nature communications · 2020Article
- Apoptotic cell death regulation in neurons.The FEBS journal · 2019Review
- A neuroprotective agent that inactivates prodegenerative TrkA and preserves mitochondria.The Journal of cell biology · 2017Article
- Programmed cell death during neuronal development: the sympathetic neuron model.Cell death and differentiation · 2014Review
- Synergistic cytotoxicity of gemcitabine, clofarabine and edelfosine in lymphoma cell lines.Blood cancer journal · 2014Article
- The ROS/JNK/ATF2 pathway mediates selenite-induced leukemia NB4 cell cycle arrest and apoptosis in vitro and in vivo.Cell death & disease · 2013Article
- Multiple mechanisms repress N-Bak mRNA translation in the healthy and apoptotic neurons.Cell death & disease · 2013Article
- SYK inhibition modulates distinct PI3K/AKT- dependent survival pathways and cholesterol biosynthesis in diffuse large B cell lymphomas.Cancer cell · 2013Article
- ATF4 orchestrates a program of BH3-only protein expression in severe hypoxia.Molecular biology reports · 2012Article
- ATF2 - at the crossroad of nuclear and cytosolic functions.Journal of cell science · 2012Article
- Global analysis of gene expression in NGF-deprived sympathetic neurons identifies molecular pathways associated with cell death.BMC genomics · 2011Article
- NF-Y is essential for expression of the proapoptotic bim gene in sympathetic neurons.Cell death and differentiation · 2011Article
- Egr-1 transactivates Bim gene expression to promote neuronal apoptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The death of sympathetic neurons after nerve growth factor (NGF) withdrawal requires de novo gene expression. Dp5 was one of the first NGF withdrawal-induced genes to be identified and it encodes a proapoptotic BH3-only member of the Bcl-2 family. To study how dp5 transcription is regulated by NGF withdrawal we cloned the regulatory regions of the rat dp5 gene and constructed a series of dp5-luciferase reporter plasmids. In microinjection experiments with sympathetic neurons we found that three regions of dp5 contribute to its induction after NGF withdrawal: the promoter, a conserved region in the single intron, and sequences in the 3' untranslated region of the dp5 mRNA. A construct containing all three regions is efficiently activated by NGF withdrawal and, like the endogenous dp5, its induction requires mixed-lineage kinase (MLK) and c-Jun N-terminal kinase (JNK) activity. JNKs phosphorylate the AP-1 transcription factor c-Jun, and thereby increase its activity. We identified a conserved ATF site in the dp5 promoter that binds c-Jun and ATF2, which is critical for dp5 promoter induction after NGF withdrawal. These results suggest that part of the mechanism by which the MLK-JNK-c-Jun pathway promotes neuronal apoptosis is by activating the transcription of the dp5 gene.
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