ArticleMolecular and cellular neurosciences2008
A novel role for jun N-terminal kinase signaling in olfactory sensory neuronal death.
Article in Molecular and cellular neurosciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 10 citations in OpenAlex.
- Programmed Cell Death in Chronic Rhinosinusitis.Clinical and translational allergy · 2026Review
- Inhibition of focal adhesion kinase increases adult olfactory stem cell self-renewal and neuroregeneration through ciliary neurotrophic factor.Stem cell research · 2020Article
- Acute N-Acetylcysteine Administration Ameliorates Loss of Olfactory Neurons Following Experimental Injury In Vivo.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Olfactory loss in chronic rhinosinusitis is associated with neuronal activation of c-Jun N-terminal kinase.International forum of allergy & rhinology · 2018Article
- Growth inhibition of malignant glioblastoma by DING protein.Journal of neuro-oncology · 2012Article
- ATP mediates neuroprotective and neuroproliferative effects in mouse olfactory epithelium following exposure to satratoxin G in vitro and in vivo.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Antioxidant-like effects and protective action of transcranial magnetic stimulation in depression caused by olfactory bulbectomy.Neurochemical research · 2010Article
- Combination chemical genetics.Nature chemical biology · 2008Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Olfactory sensory neurons (OSNs) represent a unique population of neurons in which death and regeneration are ongoing throughout adulthood, a feature that makes them an attractive model cell type for the investigation of neuronal death. However, the mechanism by which OSNs die remains elusive. Therefore, we developed a culture system for studying pathways involved in OSN death. Here, we show that inhibition of transcription or translation, by actinomycin D or cycloheximide, respectively, suppresses pathways leading to death, prolonging the survival of OSNs in culture. We discovered that caspase activity and jun N-terminal kinase (JNK) signaling both play a role in OSN death, and inhibition of JNK activity suppresses effector caspase (caspase-3) activation. Results from studies in culture were confirmed in vivo, in a mouse bulbectomy-induced OSN death model. These findings provide new insights into the nature of OSN death and a means of studying OSNs in vitro.
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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.