ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Phosphorylation of c-Jun in avian and mammalian motoneurons in vivo during programmed cell death: an early reversible event in the apoptotic cascade.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. 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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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- In toto imaging of glial JNK signaling during larval zebrafish spinal cord regeneration.Development (Cambridge, England) · 2023Article
- Lidocaine Ameliorates Diabetic Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats through Modulating the c-Jun Signaling Pathway.Contrast media & molecular imaging · 2022Article
- Review
- Motor neuron loss in SMA is not associated with somal stress-activated JNK/c-Jun signaling.Human molecular genetics · 2019Article
- The Y172 Monoclonal Antibody Against p-c-Jun (Ser63) Is a Marker of the Postsynaptic Compartment of C-Type Cholinergic Afferent Synapses on Motoneurons.Frontiers in cellular neuroscience · 2019Article
- The Effect of Minimally Invasive Hematoma Aspiration on the JNK Signal Transduction Pathway after Experimental Intracerebral Hemorrhage in Rats.International journal of molecular sciences · 2016Article
- ZPK/DLK and MKK4 form the critical gateway to axotomy-induced motoneuron death in neonates.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Induction of phosphorylated c-Jun in neonatal spinal motoneurons after axonal injury is coincident with both motoneuron death and regeneration.Journal of anatomy · 2014Article
- CLAC-P/collagen type XXV is required for the intramuscular innervation of motoneurons during neuromuscular development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Valproic acid protects neurons and promotes neuronal regeneration after brachial plexus avulsion.Neural regeneration research · 2013Article
- Astragalus injection protects cerebral ischemic injury by inhibiting neuronal apoptosis and the expression of JNK3 after cerebral ischemia reperfusion in rats.Behavioral and brain functions : BBF · 2013Article
- Drp1-mediated mitochondrial dynamics and survival of developing chick motoneurons during the period of normal programmed cell death.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- P75 and phosphorylated c-Jun are differentially regulated in spinal motoneurons following axotomy in rats.Neural regeneration research · 2012Article
- Glucocorticoid receptor and myocyte enhancer factor 2 cooperate to regulate the expression of c-JUN in a neuronal context.Journal of molecular neuroscience : MN · 2012Article
- Effect of Strychinine, a Glycine Inhibitor, on the Programmed Cell Death of Motoneurons during the Chick Development.Experimental neurobiology · 2011Article
- ZPK/DLK, a mitogen-activated protein kinase kinase kinase, is a critical mediator of programmed cell death of motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Loss of ATF2 function leads to cranial motoneuron degeneration during embryonic mouse development.PloS one · 2011Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
c-Jun is a transcription factor that is involved in various cellular events, including apoptotic cell death. For example, phosphorylation of c-Jun is one of the earliest biochemical changes detected in dying sympathetic neurons after NGF deprivation in vitro. However, currently, it is not known whether a similar molecular event is involved in the developmental programmed cell death (PCD) of neurons in vivo. We observed that only a subpopulation of motoneurons (MNs) exhibit c-Jun phosphorylation during the PCD period in chick [embryonic day 5 (E5)-E12] and mouse (E13-E18) embryos. Experimental perturbation of MN survival-promoting signals by limb bud removal (reduced signals) or by activity blockade (increased signals) in the chick embryo demonstrated that the presence of those signals is negatively correlated with the number of c-Jun-phosphorylated MNs. This suggests that insufficient survival signals (e.g., neurotrophic factors) may induce c-Jun phosphorylation of MNs in vivo. Consistent with the idea that c-Jun phosphorylation is a reversible event during normal PCD of MNs, we found that c-Jun phosphorylation was transiently observed in a subpopulation of mouse MNs rescued from PCD by deletion of the proapoptotic gene Bax. Inhibition of c-Jun signaling significantly reduced MN death in chick embryo, indicating that activation of c-Jun signaling is necessary for the PCD of MNs. Together, c-Jun phosphorylation appears to be required for the initiation of an early and reversible event in the intracellular PCD cascade in vivo after loss of survival-promoting signals such as neurotrophic factors.
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