ArticleProceedings of the National Academy of Sciences of the United States of America2018
HSP90 is a chaperone for DLK and is required for axon injury signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 44 citations in OpenAlex.
- Ergothioneine Modulates Inflammatory Signaling in LPS-Stimulated RAW 264.7 Macrophages.Cell biochemistry and biophysics · 2026Article
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Multiple regulators constrain the abundance of Caenorhabditis elegans DLK-1 in ciliated sensory neurons.G3 (Bethesda, Md.) · 2025Article
- Neurons Are Not All the Same: Diversity in Neuronal Populations and Their Intrinsic Responses to Spinal Cord Injury.ASN neuro · 2025Review
- Article
- Review
- The response of Dual-leucine zipper kinase (DLK) to nocodazole: Evidence for a homeostatic cytoskeletal repair mechanism.PloS one · 2024Article
- Amino-terminal proteolytic fragment of the axon growth inhibitor Nogo-A (Rtn4A) is upregulated by injury and promotes axon regeneration.The Journal of biological chemistry · 2023Article
- An intraflagellar transport dependent negative feedback regulates the MAPKKK DLK-1 to protect cilia from degeneration.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Transcriptomic Analysis of the Effect of Torin-2 on the Central Nervous System ofInternational journal of molecular sciences · 2023Article
- Organismal Roles of Hsp90.Biomolecules · 2023Review
- Autophagy protein ULK1 interacts with and regulates SARM1 during axonal injury.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- DLK-Dependent Biphasic Reactivation of Herpes Simplex Virus Latency Established in the Absence of Antivirals.Journal of virology · 2022Article
- A Critical Role for DLK and LZK in Axonal Repair in the Mammalian Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Functional analysis of a novel de novo variant in PPP5C associated with microcephaly, seizures, and developmental delay.Molecular genetics and metabolism · 2022Article
- Palmitoylation couples the kinases DLK and JNK3 to facilitate prodegenerative axon-to-soma signaling.Science signaling · 2022Article
- Protein phosphatase 2A restrains DLK signaling to promote proper Drosophila synaptic development and mammalian cortical neuron survival.Neurobiology of disease · 2022Article
- A small heat shock protein, GmHSP17.9, from nodule confers symbiotic nitrogen fixation and seed yield in soybean.Plant biotechnology journal · 2022Article
- Analysis of neuronal injury transcriptional response identifies CTCF and YY1 as co-operating factors regulating axon regeneration.Frontiers in molecular neuroscience · 2022Article
- In Vivo Gene Delivery of STC2 Promotes Axon Regeneration in Sciatic Nerves.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Peripheral nerve injury induces a robust proregenerative program that drives axon regeneration. While many regeneration-associated genes are known, the mechanisms by which injury activates them are less well-understood. To identify such mechanisms, we performed a loss-of-function pharmacological screen in cultured adult mouse sensory neurons for proteins required to activate this program. Well-characterized inhibitors were present as injury signaling was induced but were removed before axon outgrowth to identify molecules that block induction of the program. Of 480 compounds, 35 prevented injury-induced neurite regrowth. The top hits were inhibitors to heat shock protein 90 (HSP90), a chaperone with no known role in axon injury. HSP90 inhibition blocks injury-induced activation of the proregenerative transcription factor cJun and several regeneration-associated genes. These phenotypes mimic loss of the proregenerative kinase, dual leucine zipper kinase (DLK), a critical neuronal stress sensor that drives axon degeneration, axon regeneration, and cell death. HSP90 is an atypical chaperone that promotes the stability of signaling molecules. HSP90 and DLK show two hallmarks of HSP90-client relationships: (
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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.