Publications
63
Citations
2,606
Est. group size
~9
Recurring co-author estimate
Active years
23
Publishing since 2003
Jill C. Fehrenbacher studies how the nervous system detects pain and how nerves are damaged, with a particular focus on chemotherapy-induced peripheral neuropathy (nerve damage caused by cancer drugs such as paclitaxel). The work uses laboratory models (cultured sensory neurons and rodents) to understand the molecular signals behind pain sensitivity, inflammation, and nerve injury, and to identify potential drug targets. Recent projects also explore roles for nerve signaling molecules like calcitonin gene-related peptide in tissues such as the prostate.
Publication output was steady at roughly 2-4 papers per year across most of the decade, with a notable spike in 2024.
Generated by claude-opus-4-8 from public bibliographic data · Jul 11, 2026
- Syntaxin1A overexpression and pain insensitivity in individuals with 7q11.23 duplication syndrome
JCI Insight · 2024
- Sensory innervation in the prostate and a role for calcitonin gene-related peptide in prostatic epithelial proliferation
Frontiers in Molecular Neuroscience · 2024
- Oxidative DNA Damage: A Role in Altering Neuronal Function
Journal of Cellular Signaling · 2022
- Models of Inflammation: Carrageenan‐ or Complete Freund's Adjuvant (CFA)–Induced Edema and Hypersensitivity in the Rat
Current Protocols · 2021
- Models of Inflammation: Carrageenan Air Pouch
Current Protocols · 2021
- Chemotherapy-Induced Peripheral Neuropathy
Elsevier eBooks · 2021
- Pathogenesis of paclitaxel-induced peripheral neuropathy: A current review of in vitro and in vivo findings using rodent and human model systems
2020
- Pathogenesis of paclitaxel-induced peripheral neuropathy: A current review of in vitro and in vivo findings using rodent and human model systems
Experimental Neurology · 2019
- Novel first-in-class small molecule targeting APE1/Ref-1 to prevent and treat chemotherapy-induced peripheral neuropathy (CIPN).
Journal of Clinical Oncology · 2018
- Paclitaxel inhibits the activity and membrane localization of PKCα and PKCβI/II to elicit a decrease in stimulated calcitonin gene-related peptide release from cultured sensory neurons
Molecular and Cellular Neuroscience · 2017
- DNA damage mediates changes in neuronal sensitivity induced by the inflammatory mediators, MCP-1 and LPS, and can be reversed by enhancing the DNA repair function of APE1
Neuroscience · 2017
- Paclitaxel inhibits the activity and membrane localization of PKCα and PKCβI/II to elicit a decrease in stimulated calcitonin gene-related peptide release from cultured sensory neurons
Author eBooks · 2017
- Challenges and opportunities identifying therapeutic targets for chemotherapy-induced peripheral neuropathy resulting from oxidative DNA damage
PMC · 2017
- DNA damage mediates changes in neuronal sensitivity induced by the inflammatory mediators, MCP-1 and LPS, and can be reversed by enhancing the DNA repair function of APE1
Author eBooks · 2017
- Nerve growth factor alters microtubule targeting agent-induced neurotransmitter release but not MTA-induced neurite retraction in sensory neurons
Experimental Neurology · 2016
- Current Osteoporosis Reports×10
- Proceedings of IMPRS×5
- PMC×3
- Experimental Neurology×2
- Bone×2
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 11, 2026.
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