K
Kurt E. Schaecher
Researcher at Medical University of South Carolina
Publications - 12
Citations - 801
Kurt E. Schaecher is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Calpain & Myelin. The author has an hindex of 12, co-authored 12 publications receiving 776 citations. Previous affiliations of Kurt E. Schaecher include Uniformed Services University of the Health Sciences.
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Journal ArticleDOI
A putative mechanism of demyelination in multiple sclerosis by a proteolytic enzyme, calpain.
TL;DR: Because calpain degrades all major myelin proteins, the increased activity and expression of this proteinase may play a critical role in myelinolysis in autoimmune demyelinating diseases such as MS.
A putative mechanism of demyelination in multiple sclerosis by a proteolytic enzyme, calpain (calcium-activated neutral proteinaseyexperimental allergic encephalomyelitisycalpastatinyParkinson's diseaseyAlzheimer's disease)
TL;DR: In this article, the authors evaluated calpain activity and expression (at translational and transcriptional levels) in white matter from human patients with MS and Parkinson's and Alzheimer's diseases and compared with that of normal white matter.
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Early induction of secondary injury factors causing activation of calpain and mitochondria-mediated neuronal apoptosis following spinal cord injury in rats.
J. Michael Wingrave,Kurt E. Schaecher,Eric A. Sribnick,Gloria G. Wilford,Swapan K. Ray,Debra J. Hazen-Martin,Edward L. Hogan,Naren L. Banik +7 more
TL;DR: In this paper, a 40 gram-centimeter force (g-cm) injury was induced in rats by a weight-drop method and allowed to progress for 4 hours, showing an increase in intracellular free calcium (Ca(2+)) levels.
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The effects of calpain inhibition on IkB alpha degradation after activation of PBMCs: identification of the calpain cleavage sites.
TL;DR: It is suggested that calpain plays an important role in IkBα degradation, a crucial event in T cell activation, andCalpeptin, a calpain inhibitor, inhibited IkB α degradation in a time- and dose-dependent manner.
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Mechanism of Myelin Breakdown in Experimental Demyelination: A Putative Role for Calpain
TL;DR: Subsequent studies revealed increased calpain activity and expression in the glial and inflammatory cells concomitant with loss of axon and myelin proteins, suggesting a crucial role for calpain in demyelinating diseases.