ArticleCurrent biology : CB2017
Death Receptor 6 Promotes Wallerian Degeneration in Peripheral Axons.
Article in Current biology : CB, 2017. 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 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Wallerian Degeneration and Nerve Regeneration-A Review of Cellular and Molecular Events.International journal of molecular sciences · 2026Review
- Article
- The Intricate Role of Caspase-6 and Death Receptor-6 in Neurodegenerative Diseases.Cell biochemistry and biophysics · 2026Review
- Deletion of murineScience translational medicine · 2025Article
- Identification of New Ciliary Signaling Pathways in the Brain and Insights into Neurological Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Nerve growth factor signaling tunes axon maintenance protein abundance and kinetics of Wallerian degeneration.Molecular biology of the cell · 2025Article
- Nerve Growth Factor Signaling Tunes Axon Maintenance Protein Abundance and Kinetics of Wallerian Degeneration.bioRxiv : the preprint server for biology · 2025Article
- An induced pluripotent stem cell-based model identifies molecular targets of vincristine neurotoxicity.Disease models & mechanisms · 2022Article
- Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022Review
- Baculoviral inhibitor of apoptosis protein repeat-containing protein 3 delays early Wallerian degeneration after sciatic nerve injury.Neural regeneration research · 2022Article
- The sympathetic nervous system in development and disease.Nature reviews. Neuroscience · 2021Review
- LRSAM1 and the RING domain: Charcot-Marie-Tooth disease and beyond.Orphanet journal of rare diseases · 2021Review
- p53 is required for nuclear but not mitochondrial DNA damage-induced degeneration.Cell death & disease · 2021Article
- Intraoperative single administration of neutrophil peptide 1 accelerates the early functional recovery of peripheral nerves after crush injury.Neural regeneration research · 2020Article
- A glycolytic shift in Schwann cells supports injured axons.Nature neuroscience · 2020Article
- Regulation of degenerative spheroids after injury.Scientific reports · 2020Article
- Molecular dissection of TNFR-TNFα bidirectional signaling reveals both cooperative and antagonistic interactions with p75 neurotrophic factor receptor in axon patterning.Molecular and cellular neurosciences · 2020Article
- Novel role of SARM1 mediated axonal degeneration in the pathogenesis of rabies.PLoS pathogens · 2020Article
- Proapoptotic Mitochondrial Carrier Homolog Protein PSAP Mediates Death Receptor 6 Induced Apoptosis.Journal of Alzheimer's disease : JAD · 2020Article
- A Microfluidic Culture Platform to Assess Axon Degeneration.Methods in molecular biology (Clifton, N.J.) · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Axon degeneration during development is required to sculpt a functional nervous system and is also a hallmark of pathological insult, such as injury [1, 2]. Despite similar morphological characteristics, very little overlap in molecular mechanisms has been reported between pathological and developmental degeneration [3-5]. In the peripheral nervous system (PNS), developmental axon pruning relies on receptor-mediated extrinsic degeneration mechanisms to determine which axons are maintained or degenerated [5-7]. Receptors have not been implicated in Wallerian axon degeneration; instead, axon autonomous, intrinsic mechanisms are thought to be the primary driver for this type of axon disintegration [8-10]. Here we survey the role of neuronally expressed, paralogous tumor necrosis factor receptor super family (TNFRSF) members in Wallerian degeneration. We find that an orphan receptor, death receptor 6 (DR6), is required to drive axon degeneration after axotomy in sympathetic and sensory neurons cultured in microfluidic devices. We sought to validate these in vitro findings in vivo using a transected sciatic nerve model. Consistent with the in vitro findings, DR6
Indexed as
Identifiers
What OpenQuestion holds
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.