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Dennis J. Zeh

ORCID: 0009-0006-3070-0114
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About
Contact & Profiles
A5102867967
Research Areas
  • Mitochondrial Function and Pathology
  • Autophagy in Disease and Therapy
  • Muscle metabolism and nutrition
  • Traumatic Brain Injury Research
  • Biochemical effects in animals

University of Pittsburgh
 2023-2024

VA Pittsburgh Healthcare System
 2023

 Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice
OPENALEX - Publications 
Zhiping Mi Jie Ma Dennis J. Zeh Marie E. Rose Jeremy Henchir and 5 more Hao Liu Xiecheng Ma Guodong Cao C. Edward Dixon Steven H. Graham

10.1016/j.expneurol.2023.114650 article EN publisher-specific-oa Experimental Neurology 2023-12-12
 Abolishing UCHL1’s hydrolase activity exacerbates ischemia-induced axonal injury and functional deficits in mice
OPENALEX - Publications 
Zhiping Mi Nadya Povysheva Marie E. Rose Jie Ma Dennis J. Zeh and 3 more Nikitha Harikumar Mohammad Iqbal H. Bhuiyan Steven H. Graham

Ubiquitin C-terminal hydrolase L1 (UCHL1) is a neuronal protein important in maintaining axonal integrity and motor function may be the pathogenesis of many neurological disorders. UCHL1 ameliorate acute injury improve recovery after cerebral ischemia. In current study, hypothesis that UCHL1’s activity underlies its effect tested ischemic injury. Hydrolase was inhibited by treatment with inhibitor or employing knockin mice bearing mutation active site (C90A). Ischemic induced oxygen-glucose...

10.1177/0271678x241258809 article EN Journal of Cerebral Blood Flow & Metabolism 2024-06-04
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