ArticleProceedings of the National Academy of Sciences of the United States of America2021
Pathogenic role of delta 2 tubulin in bortezomib-induced peripheral neuropathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. 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 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Towards a systems-level view of the microtubule cytoskeleton and its functions in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- Neuronal toxicity and recovery from early bortezomib-induced neuropathy: blood-nerve barrier dysfunction without dorsal root ganglion damage.British journal of anaesthesia · 2026Article
- Decoding chemotherapy-induced peripheral neuropathy: ion channels, disease models, and future directions.Frontiers in pharmacology · 2026Review
- Preventing neuropathy and improving anticancer chemotherapy with a carbazole-based compound.Science advances · 2025Article
- Paclitaxel neurotoxicity is triggered by epidermal EG5-dependent microtubule fasciculation and X-ROS formation.Research square · 2025Article
- Recent Advances in Diagnosis, Management, Treatment, and Prevention of Neuropathies in Cancer Patients.Current neurology and neuroscience reports · 2025Review
- Axon-specific microtubule regulation drives asymmetric regeneration of sensory neuron axons.eLife · 2025Article
- Emerging roles for tubulin PTMs in neuronal function and neurodegenerative disease.Current opinion in neurobiology · 2025Review
- Effects of a Cannabinoid-Based Phytocomplex (Pain ReliefAnimals : an open access journal from MDPI · 2025Article
- Bortezomib-induced peripheral neuropathy: from molecular mechanisms to clinical management.Frontiers in pharmacology · 2025Review
- MFN2 coordinates mitochondria motility with α-tubulin acetylation and this regulation is disrupted in CMT2A.iScience · 2024Article
- Current understanding of the molecular mechanisms of chemotherapy-induced peripheral neuropathy.Frontiers in molecular neuroscience · 2024Review
- Bortezomib Is Toxic but Induces Neurogenesis and Inhibits TUBB3 Degradation in Rat Neural Stem Cells.Biomolecules & therapeutics · 2024Article
- Targeting dorsal root ganglia for chemotherapy-induced peripheral neuropathy: from bench to bedside.Therapeutic advances in neurological disorders · 2024Review
- Axonal degeneration in chemotherapy-induced peripheral neurotoxicity: clinical and experimental evidence.Journal of neurology, neurosurgery, and psychiatry · 2023Review
- A family of carboxypeptidases catalyzing α- and β-tubulin tail processing and deglutamylation.Science advances · 2023Article
- Skin Extracellular Matrix Breakdown Following Paclitaxel Therapy in Patients with Chemotherapy-Induced Peripheral Neuropathy.Cancers · 2023Article
- Role of tubulin post-translational modifications in peripheral neuropathy.Experimental neurology · 2023Review
- Review
- From bench to bedside: reversing established antibody responses and desensitization.Current opinion in organ transplantation · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
The pathogenesis of chemotherapy-induced peripheral neuropathy (CIPN) is poorly understood. Here, we report that the CIPN-causing drug bortezomib (Bort) promotes delta 2 tubulin (D2) accumulation while affecting microtubule stability and dynamics in sensory neurons in vitro and in vivo and that the accumulation of D2 is predominant in unmyelinated fibers and a hallmark of bortezomib-induced peripheral neuropathy (BIPN) in humans. Furthermore, while D2 overexpression was sufficient to cause axonopathy and inhibit mitochondria motility, reduction of D2 levels alleviated both axonal degeneration and the loss of mitochondria motility induced by Bort. Together, our data demonstrate that Bort, a compound structurally unrelated to tubulin poisons, affects the tubulin cytoskeleton in sensory neurons in vitro, in vivo, and in human tissue, indicating that the pathogenic mechanisms of seemingly unrelated CIPN drugs may converge on tubulin damage. The results reveal a previously unrecognized pathogenic role for D2 in BIPN that may occur through altered regulation of mitochondria motility.
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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.