基本信息
views: 5
Career Trajectory
Bio
Dr. Hollis received his Ph.D. from the University of California, San Diego (UCSD) Neurosciences Graduate Program in 2002. At UCSD, he trained under Mark Tuszynski, M.D., Ph.D., in the field of spinal cord injury repair. His studies on the corticospinal pathway, the principal motor system in primates, demonstrated that the application of developmentally relevant cues was insufficient for mediating regeneration of the corticospinal motor axons (Hollis et al. Exp Neurol 2009). Rather, he found that by utilizing a gene therapy approach, he could switch the intrinsic cell response from one mediating survival to one inducing axonal regeneration (Hollis et al. PNAS 2009). This was the first work demonstrating a gene therapy approach to modulate the intrinsic growth potential of this critical motor pathway.
In 2009, Dr. Hollis joined the laboratory of Yimin Zou, Ph.D. in the Division of Biological Sciences at UCSD. In the Zou laboratory, he established a spinal cord injury program to study the effects of the Wnt signaling pathway, a critical mediator of spinal cord axon guidance, after injury. He found that ascending sensory axons were sensitized to endogenous Wnt signaling after spinal cord injury and that inhibition of this system was sufficient to induce axonal regeneration and plasticity. Additionally, he found that by blocking Wnt signaling, plasticity of sensory and of descending corticospinal motor axons could mediate functional recovery dependent upon those two systems in rodent models of spinal cord injury.
His work in the Zou lab concluded with the initial studies on how motor cortex incorporates induced axon regeneration within the spinal cord after injury. Through the use of optogenetic mapping of motor output, he demonstrated that reorganization of cortical motor maps were coincident with the axon plasticity and enhanced recovery of corticospinal function observed upon genetic deletion of inhibitory Wnt signaling (Hollis et al. Nat Neurosci 2016).
In 2009, Dr. Hollis joined the laboratory of Yimin Zou, Ph.D. in the Division of Biological Sciences at UCSD. In the Zou laboratory, he established a spinal cord injury program to study the effects of the Wnt signaling pathway, a critical mediator of spinal cord axon guidance, after injury. He found that ascending sensory axons were sensitized to endogenous Wnt signaling after spinal cord injury and that inhibition of this system was sufficient to induce axonal regeneration and plasticity. Additionally, he found that by blocking Wnt signaling, plasticity of sensory and of descending corticospinal motor axons could mediate functional recovery dependent upon those two systems in rodent models of spinal cord injury.
His work in the Zou lab concluded with the initial studies on how motor cortex incorporates induced axon regeneration within the spinal cord after injury. Through the use of optogenetic mapping of motor output, he demonstrated that reorganization of cortical motor maps were coincident with the axon plasticity and enhanced recovery of corticospinal function observed upon genetic deletion of inhibitory Wnt signaling (Hollis et al. Nat Neurosci 2016).
Research Interests
Papers共 29 篇Author StatisticsCo-AuthorSimilar Experts
By YearBy Citation主题筛选期刊级别筛选合作者筛选合作机构筛选
时间
引用量
主题
期刊级别
合作者
合作机构
biorxiv(2024)
Jaclyn T Eisdorfer, Josh Thackray,Thomas Theis,Ana Vivinetto,Matthew T Ricci,Sherry Lin, Olisemeka Oputa, Alana M Martinez, Hannah D Nacht,Monica Tschang, Malaika Mahmood,Ashley Tucker,
biorxiv(2024)
bioRxiv (Cold Spring Harbor Laboratory) (2022)
bioRxiv (Cold Spring Harbor Laboratory) (2022)
The Journal of neuroscience : the official journal of the Society for Neuroscienceno. 49 (2021): 10148-10160
Load More
Author Statistics
Co-Author
Co-Institution
D-Core
- 合作者
- 学生
- 导师
Data Disclaimer
The page data are from open Internet sources, cooperative publishers and automatic analysis results through AI technology. We do not make any commitments and guarantees for the validity, accuracy, correctness, reliability, completeness and timeliness of the page data. If you have any questions, please contact us by email: report@aminer.cn