ArticleScientific reports2019
c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Pooled it
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Oxidative Stress Suppresses Trk Signaling While Stimulating JNK-Mediated Endocytosis and Cleavage of p75Journal of neurochemistry · 2025Article
- ProNGF elicits retrograde axonal degeneration of basal forebrain neurons through p75Science signaling · 2024Article
- PLC-γ-CaFrontiers in molecular neuroscience · 2024Article
- Nerve Growth Factor and Autoimmune Diseases.Current issues in molecular biology · 2023Review
- Article
- Genetic knockout ofFrontiers in cellular neuroscience · 2023Article
- Molecular-Scale Dynamics of Long Range Retrograde Brain-Derived Neurotrophic Factor Transport Shaped by Cellular Spatial Context.Frontiers in neuroscience · 2022Article
- An Shen Ding Zhi Ling Ameliorates the Symptoms of Attention Deficit Hyperactivity Disorder via Modulating Brain-Derived Neurotrophic Factor-Related Signaling Pathways.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The sympathetic nervous system in development and disease.Nature reviews. Neuroscience · 2021Review
- A CRMP4-dependent retrograde axon-to-soma death signal in amyotrophic lateral sclerosis.The EMBO journal · 2021Article
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- TrkA-mediated endocytosis of p75-CTF prevents cholinergic neuron death upon γ-secretase inhibition.Life science alliance · 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
- The Rab5-Rab11 Endosomal Pathway is Required for BDNF-Induced CREB Transcriptional Regulation in Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Herpes Simplex Virus, Alzheimer's Disease and a Possible Role for Rab GTPases.Frontiers in cell and developmental biology · 2019Article
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes. Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to p75 signaling has not been established. Using compartmentalized sympathetic neuronal cultures (CSCGs) as a model, we observed that the addition of BDNF to axons increased the transport of p75 and induced death of sympathetic neurons in a dynein-dependent manner. In cell bodies, internalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling in neurons. Additionally, the activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling. In axons, JNK and Rab5 were required for retrograde transport and death signaling mediated by axonal BDNF-p75 in CSCGs. JNK was also required for the proper axonal transport of p75-positive endosomes. Thus, our findings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent neuronal death signals.
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