ArticleThe Journal of cell biology2002
c-jun is essential for sympathetic neuronal death induced by NGF withdrawal but not by p75 activation.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 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.
The trial behind it
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Who cites it
46 citing papers in PubMed, 121 citations in OpenAlex.
- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- Chemogenetic neuronal silencing decouples c-Jun activation from cell death in the temporal cortex.The European journal of neuroscience · 2024Article
- Neurotrophin Analog ENT-A044 Activates the p75 Neurotrophin Receptor, Regulating Neuronal Survival in a Cell Context-Dependent Manner.International journal of molecular sciences · 2023Article
- Article
- Metabolic Control of Sensory Neuron Survival by the p75 Neurotrophin Receptor in Schwann Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Long-distance regressive signaling in neural development and disease.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- c-Jun N-terminal Kinase Mediates Ligand-independent p75Neuroscience · 2021Article
- Retrograde Degenerative Signaling Mediated by the p75 Neurotrophin Receptor Requires p150Developmental cell · 2018Article
- Neurotrophin Responsiveness of Sympathetic Neurons Is Regulated by Rapid Mobilization of the p75 Receptor to the Cell Surface through TrkA Activation of Arf6.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- KIF1Bβ increases ROS to mediate apoptosis and reinforces its protein expression through OScientific reports · 2017Article
- Neuroblast differentiation during development and in neuroblastoma requires KIF1Bβ-mediated transport of TRKA.Genes & development · 2017Article
- Molecular markers of paragangliomas/pheochromocytomas.Oncotarget · 2017Review
- Targeting Neurotrophins to Specific Populations of Neurons: NGF, BDNF, and NT-3 and Their Relevance for Treatment of Spinal Cord Injury.International journal of molecular sciences · 2017Review
- Retrograde apoptotic signaling by the p75 neurotrophin receptor.Neuronal signaling · 2017Review
- XAF1 promotes neuroblastoma tumor suppression and is required for KIF1Bβ-mediated apoptosis.Oncotarget · 2016Article
- The role of Plk3 in oncogenesis.Oncogene · 2016Review
- A role for the p75 neurotrophin receptor in axonal degeneration and apoptosis induced by oxidative stress.The Journal of biological chemistry · 2014Article
- Programmed cell death during neuronal development: the sympathetic neuron model.Cell death and differentiation · 2014Review
- DLK initiates a transcriptional program that couples apoptotic and regenerative responses to axonal injury.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Induction of heat shock protein 70 (Hsp70) prevents neuregulin-induced demyelination by enhancing the proteasomal clearance of c-Jun.ASN neuro · 2012Article
Corrections and comments
- Erratum issuedGufstafson-Brown, C [corrected to Gustafson-Brown, C]
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Sympathetic neurons depend on NGF binding to TrkA for their survival during vertebrate development. NGF deprivation initiates a transcription-dependent apoptotic response, which is suggested to require activation of the transcription factor c-Jun. Similarly, apoptosis can also be induced by selective activation of the p75 neurotrophin receptor. The transcriptional dependency of p75-mediated cell death has not been determined; however, c-Jun NH2-terminal kinase has been implicated as an essential component. Because the c-jun-null mutation is early embryonic lethal, thereby hindering a genetic analysis, we used the Cre-lox system to conditionally delete this gene. Sympathetic neurons isolated from postnatal day 1 c-jun-floxed mice were infected with an adenovirus expressing Cre recombinase or GFP and analyzed for their dependence on NGF for survival. Cre immunopositive neurons survived NGF withdrawal, whereas those expressing GFP or those uninfected underwent apoptosis within 48 h, as determined by DAPI staining. In contrast, brain-derived neurotrophic factor (BDNF) binding to p75 resulted in an equivalent level of apoptosis in neurons expressing Cre, GFP, and uninfected cells. Nevertheless, cycloheximide treatment prevented BDNF-mediated apoptosis. These results indicate that whereas c-jun is required for apoptosis in sympathetic neurons on NGF withdrawal, an alternate signaling pathway must be induced on p75 activation.
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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.